Autacoids
uterine
PGE2 + PGF2
dinoprostone (PGE2)
dinoprost (PGF2)
carboprost (synthetic
analog)
vascular
PGI2 and PGE2
TXA2, LT’s
airway
PGF2, TXA2, LT’s
PGI2, PGE2
gastric acid sec’n
PGE2, PGI2
Misoprostol (Cytotec)
abortifacients, evacuation of uterine contents in themanagement of missed abortion or
intrauterine fetal death up to 28 weeks of gestational age.
vaginal suppository
intraamniotic injection
i.m.
Vasodilat’n
vasoconstriction. LT dilate cutaneous arterioles in acute infl.
bronchoconstriction
bronchodilation
inh. HCl sec’n. Both stim mucus and bicarb sec’n = protective effect on mucosa.
p.o., analog of PGE1. Same mech as above. S.E. intestinal cramps and diarrhea. Used in
conj. w/asprin and NSAID’s, to reduce gastric ulcers caused by them.
platelet aggregat’n
stim. Made in platelets
TXA2
inh. Made in endothelium
PGI2
infl/allergic rxns
PGE2, PGF2a, PGD2,
mediators of local pain and itching, cutaneous microvascular vasodil perm. edema.
LT’s
Wheal and flare rxns.
Ductus arteriosus
maintain patency in fetus. Asprin (COX inh) promote closure of ductus arteriosus at birth
PGI2, PGE2
COX-1 and COX-2
PG synthetase-1 = constitutive, PGS-2 inducible by cytokines, inh by antiinfl.
PGS-1(COX 1),
glucocorticoids. NSAID’s block both PGS-1 and PGS-2.
PGS-2 (COX 2)
Vasc. Perm.  and GI contr. by all.
Kinins
bradykinin*
aprotinin (Trasylol)
aspirin
glucocorticosteroids
sm.m, potent vasodil of arterioles and venules in skin, skeletal m., viscera, kidney and
brain  perm & edema, BP & reflex tachy. GI sm. m. contr & bronchoconstr.
Infl. rxns prod pain, edema and stim PMN to come in
kallikrein inh to tx acute pancreatitis and severe burn injury
 localized pain and swelling by inh COX
antiinfl.
Serotonin*
stored w/n granules after synthesis. Mixed fxs on CV. Carcinoid enterochromaffin cells
prod  5-HT  fluctuations in BP, HR and CO. 5 HT4 R (from enteric neurons) stim
peristalsis in esophagus and stomach. Pain & itching in infl., also  perm , Arterioles dil,
but postcap venules constr  edema. CNS NT. Act on 5-HT3 R on CTZ area postrema
antagonists
Methysergide (Sansert)
cyproheptadine
(periactin)
ritanserin
Ondansetron(Zofran)
5-HT2 R antag., prophylactic tx of migraine b/c 5-HT2 R in cerebral arterial sm. m.
mediate vasodil, & 5-HT1 R mediate vasoconstri. 5-HT1 agonist more effective than 5HT2 R antag.
Therapeutic tx of malignant carcinoid
5-HT2 R antag. Both anti5-HT & antiH fxs. Symptomatic tx of carcinoid and allergic
infl. rxns, also tx migraine headaches.
5 HT2 antag.  platelet aggregation
5-HT3 R antag. Anti-emetic
Granisetron (kytril)
Agonists
metoclopramide
(Reglan)
cisapride (propulsid)
sumatriptan (imitrex)
busprone (Buspar)
Reuptake inh/releasing
agents
Fenfluramine
Dexfenfluramine
(Redux)
5-HT3 R antag. Atni-emetic
5 HT4 R agonist Anti-emetic/prevents gastro-esophageal reflex.
5 HT4 R agonist
5-HT1 R agonist. Most effective tx for migraine headache
5-HT1 R agonist. Subtypes of 5-HT1 R, some cause vasoconstriction and others
anxiolytic.
also elicits direct 5 HT R agonist fxs. Act in brain to prod anxiolytic and anorexigenic.
2X as potent as fenfluramine. Effective anorexigenic. Can cause fatal pulm HTN.
Histamine*
Bound histamine (mast and basophils) in pathophys, degranulation promoted by allergic
rxns to drugs (not allergic response) basic drugs and 4’ amines (morphine, codeine,
tubocruraine, guanethidine, chloroquine) or Ag-Ab mediated allergic release (Pcn, other
antibiotics). Unbound (gastric mucosa & hrt) in normal phys.
Arteriolar dil in most vasc bedscutaneous and systematic  reflex tachy ;
chronotropic and inotropic fxs; constri of larger arteries and veins (esp. pulm) pulm
BP and edema (also due to  perm.), bronchocontri and  mucus sec’n.
GI sm. m. contr.; stim of local pain and itching, mediator of allergic and local infl rxns;
stim of gastric glands. CNS NT 1’ in hypothalamus.
Inh of allergic H release
catecholamines
(epi & iso)
Methylxanthines
(theophylline &
aminophylline)
antihistamines
diphenhydramine
(benadryl) &
demenhydrinate
(dramamine)
promethazine
cyproheptadine
chlorpheniramine
terfenadine
fexofenadine
astemizole (Hismanal)
loratadine(Claritin
Chlorpheniramine or
acrivastine +
pseudoephedrine
(semprex-D)
H2 R antag
cimetidine (Tagamet)
2 R on mast cell and basophils. Adenylate cyclase activat’n  inh degranulation. Also
causes bronchodilation
inh PDE and allow cAMP to accumulate  inh degranulation. Bronchodilat’n
H1 R  local infl, edema, vasodil/constri,  perm, H2 R  gastric sec’n
H1-R antag. Drowsiness, antimusc (dry mouth) , antiemetic, antitremor (b/c anti-chol),
anti 5 HT and.sedation. Tx also colic or G.I. hypermotility, nausea and vomiting, tremors,
and insomnia. O.D.  CNS stimconvulsions
H1 R antag. Anti-coli, safe in infants. Produce drowsiness which is desirable in infants.
H1 R antag. also anti 5 HT, tx migraine also.
H1 R antag. No S.E.’s, some drowsiness but less than any of the drugs above.
H1 R antag. NO CNS fxs and no drowsiness and sedation. Tx allergic rhinitis, acute
urticaria (itching), and drug allergies. Terfenadine (pro-drug, toxic)  fexofenadine
(active species, nontoxic) For terfenadine and astemazole only, cardiac arrhythmia can
be fatal,  conc in parent drug due to P450 inhibition. Avoid erythromyocin,
ketoconazole, and grapefruit juice (?).
terfenadine analog
Acrivaastine similar to terfenadine. This combo most effective. Pseudoephedrine
prevents drowsiness, in fact may produce CNS stim.
inh gastric acid sec’n, tx ulcer. Well tolerated but significant relapse occurs.
suicide substrate, irreversibly inh P450.
Ranitidine (Zantac)
famotidine (Pepcid)
nizatidine
proton pump inh
Omeprazole (prilosec)
Lansoprazole(prevacid)
some inhibition of P450
do not inh P450
can cause complete inh of HCl sec’n, causing achlorhydria, pH allows for bacterial
infection. For short term tx for healing and symptomatic relief of erosive esophagitis
(moderate to severe gastro-esophageal reflux) and active duodenal ulcers. Cautiously for
long term tx of path hypersec gaastric cond.
Anticoagulant, antiplatelet and fibrinolytic drugs
Heparin
Dalteparin sodium
Heparin antagonist
protamine sulfate
Orally effective
anticoag.(lipid sol)
coumarin class
Warfarin
dicumarol
phenprocoumon
Antiplatelet drugs
aspirin
accelerates interxn of antithrombin III and thrombin  inactiv. thrombin
S.C. or i.v. bolus/infusion. NOT absorbed by p.o. Does not bind to plasma prot and
remains w/n intravasc. comp’t. Hepatic metabolism (0’) and renal exc’n of unchanged
drug.
 S.E. hemorrage; thrombocytopenia of immediate and delayed onset. Also
hypersensitivity rxns, fever, alopecia, hypoaldosteronism and osteoporosis.
 Contraindicated in GI ulcers, HTN, recent neurosurgery, visceral carcinoma, spinal
anesthesia. Use caution in renal/hepatic dysfcn, prior hx of occult bleeding, taking
antipletelet drugs, oral anticoagulants.
Many basic drugs (antiH, quinidine, phenothiazines, tetracyclines) can chemically
inactivate heparin.
Goal = whole blood coagulation time 2-3x normal, or an APTT of 1.5 to 2.5 normal.
 Indicated for prophylaxis of DVT, pulm/arterial embolism, prevention of arterial
emboli arising from heart valves, MI and coronary art dz.
heparin prep for injection. 1x/day. For prophylaxis against deep vein thrombosis.
Basic prot bind to and neutralize neg. charged heparin in cases of serious hemorrhage.
Slow I.V. infusion
only work in vivo. Inh of hepatic synthesis of Vit K-dep clotting factors (prothrombin,
factors VII, IX, and X) of the intrinsic and extrinsic systems and of protein C. Actual
mechanism is to block regeneration of KH2 (active hydroquinone form of Vit K) by an
epoxide reductase.
Delayed onset of action depending on drug pharmK and t1/2 of the 4 Vit K dep clotting
factors, which must be catabolized first before anticoag effect evident. Action potentiated
by  intake of vit K/fat, or by disorders that  vit K absorption.
 S.E. hemorrhage. Rare side fxs = diarrhea, urticaria, alopecia, dermatitis
 Contraindicated in GI ulcers, thrombocytopenia, renal/hepatic dz, severe HTN,
recent neurosurgery, chronic alcoholism, pregnancy, physically hazardous
occupations. Other drugs used prior or at same time can  or  effective dosage of
anticoag.
 Indicated for prophylactic tx of arterial emboli from heart valves, cond of high
thromboembolic risk, MI and cornoary art dz.
rapidly and almost completely absorbed after p.o. Extensive plasma albumin binding 
long plasma t1/2 (1.5 days and duration of 2-5 days). Displaced by other plasma prot
bound drugs. Hepatic metabolism.
erratic and delayed p.o. absorption. Higly variable t1/2 (1.5-5 d) and duration (2-10 d)
because erratic and incomplete absorption from GI. Difficult to use clinically
long acting coumarin der. t1/2 6.5 days and duration of 1-2 wks.
prophylaxis of arterial thrombosis
Lo doses of aspirin inh platelet TXA2 formation, and hi doses inh formation of both
Ticlopidine
platelet TXA2 and endothelial PGI2(endothelial cells can synth COX).
Combo therapy w/ dipyridamole, or sulfinpyrazone
inh ADP pathway in platelets. For pts who can’t tol aspirin.
Dypridamole
dextrans
sulfinpyrazone
Nitric oxide
Fibrinolytic agents
streptokinase
urokinase
Tissue plasminogen
activator
antifibrinolytic agens
aminocaproic acid
tranexamic acid
not very effective clinically. Coronary vasodilator  platelet adhesiveness to damaged
vascular endothelium by  platelet cAMP. Does NOT alter bleeding time/platelet
aggregation.
Combo therapyw/ oral anticoagulants
glucose polymers as plasma vol expanders,  platelet adhesiveness by coating platelets
and intimal lining and by other mechanisms.
comp inh of COX. Weakly affects platelet fcn.  postinfarction “sudden death”.
inh platelet aggregation and adhesion. Nitroglycerin, nitroprusside, isosorbide dinitrate =
vasodil and anti-platelets.
lyse already formed clots
indirectly activates plasminogen. I.V., intracoronary infusion, topical.
directly activates plasminogen. I.V. and intracoronary infusion.
endogenous activator of phys. fibrinolysis. I.V.-effective thrombolytic drug
antag of plasmin, reverse effects of thrombolytic agents. I.V. or p.o
analog
Antipyretic-analgesics
salicylates (aspirin
most important)
Use: Antipyretic (central)for fever; Analgesic headache (0.6-0.9g/d), myalgia,
arthralgia, dysmenorrhea and antiinfl (peripheral)ARF, rheumatoid arthritis (5-8 g/d).
Toxicity starts w/8-10g/d or when conc exceeds 30 mg%. Mean lethal dose 20-30 g. 0’
b/c hepatic enz sat.
O.D. in adults.
 GI distressnausea, vomiting, diarrhea. Local irritation b/c weak acid, PG
synthesis gastric acid sec’n and getting rid of mucosal surface. @hi dose, stim
CTZ;
 CNS stim: tinnitus (#1 reliable sign for O.D.), dizziness, hyperapnea (both depth &
rate, reg by medulla). W/ conc, get CNS deprresp failure;
 Blood coag: internal bleeding. @ v. lo doses,  platelet aggregation by  TXA2
formation to prevent 2nd infarct. Irrev. Inh of COX. To regenerate COX, must wait
for platelets to turn over which is 6-8 d, b/c platelets can’t synth own COX. @ 
doses, hypoprothrombinemia by  vit K dep factors.
 Stim of met. rate: @ hi dose, uncouples ox. phos., generates a lot of heathigh
fever and sweating. Hyperglycemia, glucosuria, by stim glycogenolysis.  plasma
free FA by inh lipolysis
 Acid-base balance disturbances: hyperventilationresp alkalosis (#2 sign in
adult) renal compensation by  elim of bicarb (last stage in adult before death).
Urine has  K to neutralize bicarb.
Children progresses rapidly thru these stages. Then goes to hypoventilat’n b/c CNS
deprresp depresp acidosismetabolic acidosis (adding aspirin which is acid in
blood phys. rxns in bodyGet ketone bodies prod in liver). Child lingers in this
stage
 H2O/electrolyte imbalance: dehydration (diuresis b/c elim a lot of electrolytes) and
hypokalemia
Contraindicated:
 in children w/ chicken pox or influenza. Otherwise Reye’s Syndrom(liver and brain
damage)
 peptic ulcer, bleeding disorders, acute gout b/c inh exc’n of uric acid, asthma
(hypersensitive to aspirin).
 High plasma prot bindingenhance warfarin and dicumarol action(usu some residual
COX fcn. Do not want to inh it completely)hemorrhage.
choline salicylate
salicylic acid
(keratolytic)
methyl salicylate
(rubefacient
take off warts. So if taken p.o., will wipe out esophagus
causes local axonal reflex vasodil and warmth, and LT relieves tenderness ( PG5
syntnh which normally provides neg feedback to inh lipoxygenase).
Tx of salicylate O.D.




acetaminophen
(Tylenol, Tempra)
analgesic & antiyretic but NOT antiinfl.
Used in all pts contraindicated for aspirin. Basic drug absorbed in small intestine rather
than stomach.
Toxicity: @ therapeutic dose, little to no GI distress/bleeding. O.D. phase II metabolism
of benzoquinone generates F.R.  depletes GSHliver cirrhosis and kidney necrosis.
Reversible is intervene w/n 24 hrs. Tx by giving N-acetylcysteine (Mucomyst) to regen
GSH.
NSAID
salicylates
indomethacin
ibuprofen (motrin,
advil)
Ketoprofen (orudis)
fenoprofen(Nalfon)
fluribiprofen(ansaid)
naproxen (Naprosyn)
Tometin (Tolectin)
meclofenamate
(Meclomen)
mefenamic acid
(Ponstel)
piroxicam (Feldene)
diclofenac (Voltaren)
diflunisal (Dolobid)
oxaprozin (Daypro)
sulindac (Clinoril)
alkalinize urine, i.v. infusion of NaHCO3. If at endstage of OD., do not give it.
Gastric lavage with 3-5% NaHCO3, which delays salicylate absorption from GI.
Emesis w/ syrup of ipecac
delay gastric emptying/absorpt’n by milk or activated charcoal (much more
effective than previous two)
Supportive Measures;
 Correct electrolyte /H2O imbalance by i.v. fluids
 maintain good renal fcn. Use osmotic diuretic (mannitol), provided patient not
hypokalemic
 control convulsions w/lo dose sedatives (watch for resp depr)
 control high fever w/ sponge baths.
 Control hemorrhaging w/ dose of vit K and blood transfusions
 dialysis
used for rheumatoid arthritis (need hi doses. Compliance a problem. Can exacerbate
gout), ankylosing spondylitis, ARF
not used any more, pharm actions same as aspirin. (NOT need to know) Use: rheumatoid
arthritis, ankylosing spondylitis, osteoarthritis of hip, nonarticular rheumatism, acute
gouty arthritis, analgesic for dysmenorrhea. S.E.: GI distressmost ulcerogenic drug by
inh COX1 (constitutive form) more. PG inh gastric acid sec’n; severe frontal headache,
hallucinations
GI distress < aspirin b/c inh COX 2 more than COX 1, but NOT selective
dizziness @ v. high doses, skin rash rare
Drug interxns and contraind similar to aspirin, except for children w/ varicella/influenza.
more potent than ibuprofen and more toxic. Tinnitus, gastric and duodenal ulcers (some
pts more sensitive to the GI irritation), rash, fluid rention, O.D.  agranulocytosis,
aplastic anemia, acute renal failure. Aspirin prod more tinnitus than any other drug.
Lo dose can inh COX, so high dose won’t further affect platelet agg. Higher incidence of
toxicity expected, esp @ hi doses.
Good.  analgesia w/ minimal gastric irritation.
Non NSAID’s
chloroquine and
hydroxychloroquine
Gold salts
D-Pencillamine
Glucocorticoids
Not antiplatelet, or gen anti infl, or analgesic.
antimalarial drugs also for tx rheumatoid arthritis and discoid lupus erythematosus. S.E.
subacute or chronic chorioretinitis, reversible if drug stopped.
I.M. tx rheumatoid arthritis. Cause complete remission in some pts w/ severe rheumatoid
arthritis. Last resort drug b/c only 30% respond. Takes 5-10 wks to work, very toxic.
Severe S.E.: skin rash, hepatic/renal damage, blood dyscrasias (inh cell prolif in bone
marrow)
tx rheumatoid arthritis
tx rheumatoid arthritis b/c anti infl.
Gout
acute gouty arthritis
colchicine
NSAIDs
(except aspirin)
chronic tophaceous gout
allopurinol
probenecid
sulfinpyrazone
used prophylactically and therapeutically. Dramatic relief w/n 90 min. Mechanism =
binding to tubulin, inh assembly of microtubule and therefore lysosome fusion w/ other
vesicles and lysosome release. In gout, acute local pain in reaction to uric acid crystals
deposited in jts.
Slight O.D. extremely toxic:
 GI ulceration b/c it inh spindle fiber formation and cell division arrested in metaphase
 severe abdominal pain (80%)
 agranulocytosis/aplasatic anemia
 profound alopecia, but reversible as soon as drug withdrawn.
for pts who can’t tolerate colchicine. Anti infl and analgesic.
By inh xanthine oxidase,  uric acid in blood and shift equilibrium to sol form of blood.
But can ppt later acute flare-ups (sxs of acute gouty arthritis).
uricosuric agent by inh sec’n of uric acid @ lo dose & inh sec’n and reabsorption @ hi
doses. can cause acute flare-ups. Gen well tol. Used in combo with Colchicine =
colbenemid, to minimize acute flare-ups and renal damage.
uricosuric agent, also has weak gen anti infl. SE more serious than probenecid, include
GI distress and skin rash.
Asthma
Isoproterenol
Epi
Terbutaline
metaproterenol
albuterol
bitolterol
salmeterol
formoterol
ephedrine
Bronchial asthma—reversible airway obstruction
 extrinsic—allergic, in children, tx w/ anti-infl
 Intrinsic—nonallergic, nonspecific hyperreactivity, mostly in older adults. Mucosal
infl/edema, triggered by cold water, dust and exercise. Vagal component reflex
vagal discharge via local contraction and can be tx by anti-musc.
 Status asthmaticus—severe acute bronchospasm
1/2 agonist. Used therapeutically for bronchodil and inh of mediator release (2).
Must be given locally at lungs. Quick onset and metabolism. S.E: myocardial stim, hand
tremor, CNS stim. Tachyphylaxis.  ventilation/perfusion ratio because dilates
previously constricted BV in areas of poor perfusion.
b2 R agonist. Used therapeutically by inhalation and prophylactically by oral. S.E.:
hand tremor and mild cardiac stim. Reflex sympa stim not as bad as iso.
These drugs short duration of action: 1-5 hr
long duration of action: 12 hr
bronchodilation and pulm decongestant. S.E: intense CNS and cardiac stimlots of
deaths.
phenylephrine
theophylline
aminophylline
Cromolyn sodium and
nedocromil sodium
Anti infl
glucocorticoseroids
Beclomethasone
dipropionate
flunisolide
budesonide
triamcinolone
anticholinergice agents
Ipratropium bromide
N-Acetylcysteine
(Mucomyst)
Zileuton (leutol)
Zafirlukast (Accolate)
selective a1 R agonistmucosal vasoconstriction and pulm decongestion. Used with
isoprot to alleviate  vent/perf ratio &  arterial hypoxemia associ.
PDE inh. P.o. as prophylactic agent. S.E.: GI upset, CNS & cardiac stim. Very toxic,
but causes sustained inh of mediator release and bronchodil. Both methylxanthines have
low therapeutic index.
water sol salt of theophylline. Cause intense vasoconstriction. CNS stim—seizures,
convulsions. Plasma level must be closely monitored. I.v. to tx status asthmaticus.
prophylactically (takes days to work) by inhalation. Tx exercise induced asthma.
Effective in children. V. safe. Mast cell stabilizer = no degranulations, fx on mast cell >
basophil.
prophylactically by inhalation. Removes sensory n. stim and therefore vagal stim. P.O
cause severe S.E., adrenal atrophy, diabetes, cataract and ulcer. Major SE = fungal
infection in pharynx and larynx b/c inh Plipaase A2 and therefore  PG and LT, also 
cytokine prod by T-lymphocyte in airway.
Not much systemic SE
block vagally mediated bonchospasm in intrinsic asthmabronchodil. Toxicity =
inspissation of mucus and  mucociliary clearance.
prophylactically by inhalation. No serious SE b/c 4’ ammonium compound. Anti-chol
effect on bronchial sm. m. but not on epithelial cells. No insipissation effect.
Mucolytic agent. By inhalation. N-Acetylcysteine—reduces disulfide bonds in hard
mucus plus to free -SH groups.
5-lipoxygenase inhibtors. P.O.
LT-D4 R Antag
Diuretic Drugs—organic acid and base secretory systems delivers diuretics into tubular lumen.
High intrinisic activity, in proximal tubule memb, inh Na bicarb reabsorption by
Carbonic anh. inh
acetazolamide (diamox) inhibiting CA.  bicarb  hyperchloremic metab. acidosis, b/c  NaCl reabsorption
downstream. Urine alkaline.  Na exc’n   K exc’n when presented to CCT
TX:
 glaucoma by inh aq humor form’n,  intraocular p.
 Alkalinization of urineelim acidic agents, e.g. uric acid and cystine.
 Metabolic alkalosis, eg. Acute mtn sickness. Take it a few days prior to climbing to
minimize resp alkalosis by  bicarb in body.
Loop diurectics
 High intrinsic activity. inh Na+/K+/2Cl transporter in thick ascending limb, also
inh reabsorption of Mg and Ca. Inh K cycling which normally drives Mg and Ca
 furosemide*
reabsorptionhypomagnesemia but not hypocalcemia b/c Ca absorbed in DCT.
 torsemide
 exc’n of Na, Cl and Kdiuresis and hypokalemia. Prolonged hi doses bicarb
 bumetanide*
exc’n. (HOW?)
 ehtacrynic acid*
 highly bound to plasma prot. Elim unchanged in ruine and feces. Inh uric acid sec’n
in proximal tubule b/c use same transporter.
 Use: acute pulm edema, hyperkalemia, in pts w/ impaired renal fcn or acute renal
failure, CHF.
 SE: #1= rapidly circulating blood voldizziness, headache, ortho hypo.
Hyponatremia (@ hi dose or prolonged therapy, for alkalosis also), hypokalemia and
hyperuricemia. Major toxcity = hypokalemic metabolic alkalosis b/c drug  elim
of H+ (maybe hypomagnesemia )
Benzothiadiazides
 inh NaCl co-transporter in DCT, inh uric acid sec’n in proximal tubule by
(thiazide)
competitionexacerbate gout. Probenecid inh thiazide from getting into lumen
 Chlorothiazide*
by competing w/ secretory transporter.
 hydrochloro-*
thiazide
 benzthiazide
 trichlormethiazide
 chlorthalidone*
 indapamide

K sparing diuretics
Low intrinsic activity b/c low Na reabsoption here. act in cortical collecting tubule and
late distal tubule to produce mild natriuresis and diuresis but  K and H exc’n. Delayed
onset of axn. Tx essential HTN (mild), CHF, cirrhosis, states of mineralcort excess.
Used w/ thiazides or loop diuretics to minimize hypokalemia.
SE: hyperkalemia in pts w/ impaired renal fcn or  K intake, or synergistic fx in pts
taking b blockers which  renin sec’n or AT II formation (ACE inh). Hyperchloremic (?)
metabolic acidosis can develop.
sprionolactone
Aldosterone R antagonist. Synthetic steroid acts as comp antag to aldosterone.
SE: GI distress, drowsiness and reversible gynecomastia b/c blocks androgen formation.
Tx hirsuitism.
Na channel blocker. Usu Na absorp’n generates lumen-neg potential, which enhances K
and H sec’n. Amiloride is a direct vasodil also.
Given i.v.. water soluble, freely filterable, poorly reabsorbable nonelectrolytes.
USE: maintain renal fcn (urine format’n) in  renal dynamics,  intraocular P,  ICP in
surgery,  elim of ingested toxic substances.
SE:  mobilization of fluid from IC to EC comp’t  acute pulm edema and acute
CHF (when kidney can’t elim the displaced water). Also headache, nausea, vomiting and
chest pains.
Triamterene
amiloride
Osmotic diuretics
mannitol, glycerin
isosorbide
Enhanced apical Ca reabsorption on apical membrane. Possible mechanism
Na/Ca exchange in basolateral membNa elim and  Ca reabsorption. Unmask
hypercalcemia caused by hyperparatyroidism.
 SE: Hypokalemia w/dosage or prolonged therapymuscle weakness, drowsiness,
dizziness, irritability, cardiac arrhythmias, correct by giving K supplGI irritation,
can eat fruits instead. Also hypokalemic metabolic alkalosis, hyperuricemia,
hyperglycemia in diabetic pts, hyperlipidemia and allergic rxns.
 Highly bound to plasma prot. Elim unchanged, renal 60% hepatobiliary 40%
 Use: 1st line for essential HTN (mild edematous, mild to moderate HTN) b/c lo level
of diuresis, CHF, cirrhosis, idiopathic hypercalciuria.
indapamide Elim 1’ by hepatic-biliary sec’n (80%), for people w/ renal dysfcn.
Carbonic anhydrase
inh
Antianginal and vasodilator drugs
typical angina
variant angina
organic nitrate esters
nitroglycerin
(glyceryl trinitrate)
Isosorbide dinitrate
erythrityl tetranitrate
pentaerythritol
tetranitrate
organic nitrite esters
isoamyl nitrite, isobutyl
nitrite
sodium nitroprusside
 in myocardial oxygen requirement  pain
sudden coronary vasospasm  inadequate supplyeven at rest
short term therapy
 lipophilic, short acting, met to NO in vasc sm. m. Venodil   preload, major
mech for relief in typical angina, tx CHF and acute MI; arteriodil   afterload.
Both  O2 demand. Tx variant angina by coronary arteriodil.
Extensive 1st pass. Adm subling (buccal), transdermal patch, and i.v. infusion.
SE: hypotension  headache, ortho hypo, flush, relex tachy. Methemoglobinemia and
tolerance uncommon with lo dosage.
longer acting organic nitrate ester, no 1st pass metabolism, adm p.o.
Last two can be taken prophylactically
potent vasodil. I.v. infusion. Spontan. release of NO.  BP in HTN emergency or crisis
or during surgical procedures.
-adreneric R agonists
propranolol
Metoprolol
atenolol
pindolol
nadolol
Ca channels blockers
nifedipine
nicardipine
nitrendipine
nisoldipine
amlodipine
Mibefradil (Posicor)
verapamil
Diltiazem
bepridil
AntiHTN drugs
diuretics
(loop & thiazide)
vasodilators
hydralazine
Minoxidil (Rogaine)
 myocardial sympa response to stress & exercise   myocard oxygen demand. 
tolerance to exercise but also less vigorous exercise possible.
Long term therapy, used w/organic nitrate esters to offset each other’s SE’s.  block 
HR ( reflex tachy in nitroglycerin use) diastole  LVDV, LVDP (blocked by
nitroglycerin)   oxygen demand. Avoid abrupt w/drawal b/c will get upreg of  R.
Do not use nonselective  blockers for variant angina. Normally epi released during
stress acts on  2 R  vasodil.  block leads to unopposed  1 R activation by NE 
worsen coronary vasospasm.
1 R blocker
1, 2 R blocker

L-type (large in conductance) predominant in cardiac and sm. m. fxs: SA node
(brady);  AV cond vel, and  cardiac contr.   CO. Vasc sm. m > nonvasc sm
m (airway, GI, uterine, etc). Arterial sm m > venous, so ortho hypo not common SE.
 Ca channel antagonists only partially interfere w/ Ca movememnt thru R gated Ca
channels. T(secr) and N (neurons) types are less sensitive to blockade by Ca channel
blockers.
 Vasodil   SVR   BP   reflex symp stim ( not much  HR and contr b/c Ltype in hrt blocked) +  renin sec’n b/c T type not blocked   bl. Vol, edema in
obese elderly; can be  by diuretic)
 SE: brady, AV-block, card arrest, acute CHF. Less serious SE = flushing, edema,
dizziness, nausea, and constipation.
a dihydropyridine, tx both typical and variant. Also essential HTN. Vasc > heart.
Arteriodil  afterload > venodil  preload. Cornoary arteriodil stops vasospasm. Mild
myocard depr b/c  CO.
New T-type blocker (tetralol class). New analogs of nifedipine w/ longer duration of
action. Greater effect on vasc sm m than nifedipine. Tx essential HTN also. Blocks
renin sec’n   edema.
T-type channel blocker. T-type channel blocker: act on SA node  brady, does NOT 
CO. Relax arterial sm m. No reflex tachy. Tx both typical and variant   oxygen
demand.
heart > vasc. Severe neg inotropic fx and brady pts on  blockers v. sensitive to
cardiodepr fxs. NOT used for angina. For antiarrhythmia.
vasc = heart. Neg chronotropic axn most prominent. 1’ for antiarrhythmia.
used alone to tx mild-mod essential HTN. Thiazid preferred over loop unless want more
diuresis. Beware of electrolyte loss. In combo for severe HTN: Triple combo. Vasodil
BP reflex symp. Stim HR ( by  blocker ) +  renin sec’n ( by  blocker
and by diuretics, which also  bl. vol)   BP.
arterial > venous, thus ortho hypo not a problem. Never used alone. See flowchart above
b/c will have reflex tachy and renin sec’n.
regional arteriodil (renal/splanchnic), works in vivo only. Tx moderate-severe essential
HTN, by  SVR, in combo w/ diuretic and  blocker.
SE: vasodil  headache, flushing, nasal congestion, rare rxn is SLE. Mech unknown
widespread arteriodil via  gKhyperpolarization  close inward Ca channel  sm
diazoxide
nitroprusside
nifedipine
Adrenolytic agents
methyldopa
clonidine (guanabenz)
Ganglionic blockers
trimethaphan
Depletors of NT
reserpine
guanethidine
(guanadrel)
Adrenergic R antagonist
prazosin
terazosin
doxazosin
propranolol
metoprolol
atenolol
acebutolol
alprenolol
esmolol
ACE inhibitors
captopril*
enalapril*
enalaprilat
lisinopril
fosinopril
ramipril
benazepril
quinapril
perindopril
moexipril
AT II R antagonist
m relaxation. Normally K channel closed and Ca flux maintained. Tx: moderate-severe
essential HTN. SE: headache, flushing, nasal congestion, (more severe than
hydralazine) hypertrichosis (topical for hair growth, could cause hypotension if
excessive amt applied).
potent widespread arteriodilator. Mech same as above. I.V. in HTN emergencies and
to produce controlled hypotension during surgical procedures.
potent widespread vasodil (both art. & veins)
1st choice for HTN. L-type blocker. Used in combo w/ a diurectic but NOT w/  blocker
because  blocker unmasks a severe cardiac depr axn  brady, CHF, severe AV block (
CO), and arrhythmias.
central actions, agonist of  2 R.  NE release  arteriodil   BP  MILD reflex
symp stim
 venodil ortho hypo.
Tx mild-moderate essential HTN, also typical and variant angina, in combo w/
diuretics & maybe  blockers.
SE, in absence of  blockers: mild ortho hypo, mild tachy, drowsiness, nasal congestion,
dry mouth ( Ach release @ salivary gl, parotid gl swelling), and constipation ( Ach
release in GI),  ejac. Avoid abrupt w/drawal.
i.v. for HTN emergencies. No reflex b/c ganglion blocked.
for moderate-severe essential HTN, in combo w/ diuretics and cautiously w/  blocker.
lipophilic, penetrates CNS, causes depletion slowly, headache, drowsiness b/c NE
deplet’n. Dopamine depletion causes depression and Parkinsonian tremor  contraind in
depr and PD.
NO CNS fx. arteriodil BPmoderate reflex symp b/c  NE in nerves involved in
reflex symp. W/phentolamine (1,  2 blocker) get very severe reflex symp;
Venodilortho hypo.
SE: initially get  HR and BP b/c amphetamine & cocaine like action. Then get  BP 
reflex. Also get ortho hypo, nasal cong,  ejaculation, diarrhea b/c  NE to inh 2  
Ach release.
 1 blockers. For mild, moderate, severe essential HTN, in combo w/ diuretic and 
block. Moderate reflex symp stim, more serious than clonidine.
SE: moderate ortho hypo, mild tachy/palp, nasal cong, infrequent impairment of ejac.
NO CNS/GI effects.
nonselective  blocker
 1 blocker. Not helpful for essential HTN b/c it’s mainly a problem of  SVR.  depr
HR and SV, not SVR. Used w/ diuretics and vasodil to prevent reflex symp of vasodil.
Can be used alone in young adults and tx HTN brought on by stress/anxiety.
used in pts w/ renin-AT axis HTN.  BP in pts w/  renin sec’n.  BP in other pts
b/c it’s also ACE = bradykininase.  bradykinin  vasodil. Used alone or w/ diuretics,
but generally do not need diuretics, b/c renin-AT inhibited.
SE assoc. w/ captopril and enalapril  agranulocytosis/glomerulonephritis.
For all drugs, accumulation of bradykinin, an autacoid  persistent coughing in most
pts, also get angioedema and skin rash.
When used for CHF in pts w/ severe renin-AT component and  PVR marked
hypotension and  renal fcn. Must have good renal fcn to begin with.
losartan (Cozaar)
losartan &
hydrochlorothiazide
(Hyzaar)
works well in 1’ HTN, less well in essential HTN
extremely effective for essential HTN, b/c  SVR and circulating vol
Cholesterol and hypocholesterolemic drugs
to  plasma cholesterol
cholestyramine
Drug of choice for type 2a hypercholesterolemia. Bile acid sequestrant.  LDL by 20colestinpol
25%. Does NOT  TG. A 4’ ammonium anion exchange resin. P.O.  exchange Cl for
bile salts   exc’n in feces. B/c removes product  7 Ohase +  breakdown.
SE: well tol but can cause constipation. Drug interxn: interferes w/ GI absorpt’n of
many drugs. Should not take other drugs concurrently.
Niacin (nicotinic acid)
Tx hypercholest, hyperTG, & type 2b hyperlipoproteinemias.  cholest & TG, but
mainly on TG.  synth of TG   hepatic sec’n of VLDL, which give rise to LDL  
circulating LDL and thus cholesterol.  cholest (15-30%) and TG (60%)
SE:  flush + pruritus (itching), which are  by aspirin but not acetaminophen. Less
frequent are jaundice, glycosuria, hyperuricemia.
Contraindicated: hepatic dysfcn and peptic ulcer.
Tx type IIa heterozygous familial hypercholest. Inh cholest synth by inh HMG CoA
Lovastatin
Simvastatin
reductase   hepatic LDL R synth and  removal of LDL from circulation. In combo
pravastatin
with bile acid sequestrant.
fluvastatin
SE: Long term use  reversible skeletal muscle disorder of moderate to extreme
pain, which  w/ gemfibrozil use.
Contraindicated in pregnancy and lactation b/c cholest necessary for fetal and early post
natal development.
probucol
bis-phenol  LDL by producing struct altered LDL  rapidly removed from circulation.
Not ideal b/c  both LDL and HDL.
neomycin
aminoglycoside anatibiotic inh reabsorption of cholest and bile acids  moderate  in
LDL. No TG .
SE: v. toxic. Nausea, abdominal cramps, diarrhea, enterocolitis, hepatic and otic toxicity
as well.
Best used w/ niacin.
To  plasma TG
clofibrate
hypoTG by stim of lipoprot lipase  remove TG from circulation30-40% reduction.
Hypocholest by both inh of cholest synth and stim of exc’n in bile and feces.
For type 3 hyperlipoproteinemia b/c stim degradation of IDL.
Pro-drug, hydrolyzed by GI and serum esterases to clofibric acid (active species).
SE: nausea, diarhea, wt gain. More serious is gallbladder or hepatobiliary neoplasia.
These SE limit its use.
Drug interxn: dispace coumarin from plasma prot b/c it’s plasma prot bound.
Fenofibrate
benzafibrate
gemfibrozil
new and safer analogs
Tx type 2, 4 and 5 hyperlipoproteinemias. der of fibric acid.  VLDL TG by 35%+ by
inh VLDL synth by liver, and  clearance of VLDLs from circulation.  LDL some. 
HDL by stim VLDL catabolism. Used w/ lovastatin  muscle pain
Drugs for CHF
clinical managemt of
CHF
+ inotropic agent: digoxin
K sparing diuretic
vasodil: venodilator (isosorbide dinitrate) and vasodil (hydralazine)
digitalis glycosides
digoxin
digitoxin
amrinone
milrinone
dopamine
dobutamine
ACE inh: must be careful in pts w/ v. lo BP b/c further BP could  renal fcn more.
delays but not change mortality. Active species = aglycone, w/steroid nucleus and
lactone ring.
 Compare to catecholamines:  cardiac wk/oxygen consumption ratio. NO  in
cardiac metabolism of cAMP levels or HR. Myocardial performance and wk index
.
 Tx CHF, esp pts w/ concurrent supraventricular tachyarrhythmias, which
responds b/c vagomimetic action of dig by  cond vel and  ERP in AV node.
 Mechanism: inh Na/K ATPase by binding to K binding site   intracellular Na 
turns off the Na/Ca exchanger b/c Na can’t enter   Ca   intracellular bound Ca
into free form  cardiac contrac’n.
 Effect: in normal person,  SV counteracted by  HR. Vasocontriction by digitalis
prevents  CO. No diuresis because CO unchanged. In CHF, vasodil happens b/c
 reflex sympa stim and better renal and systemic perf   afterload, LVEDV and
heart size.
 Get diuresis b/c  CO and  renal flow. Get  HR b/c direct and indirect
(vagomimetic, sensitizes baroreceptor in carotid sinus,  vagal outflow 
bradycardia and AV block, fx blocked by atropine) on SA node. @ hi doses, toxic to
SA and can’t be blocked by atropine.
 Toxicity: Narrow margin of safety. Discont if toxic sxs occur. arrhythmias and
cond disturbances common.
 Less neg transmemb pot by disrupting Na/K ATPase  extrasystoles,  AP
amplitude, and  cond vel  prolonged PR interval.  Ca   automaticity. 
ERP in AV node, but  in Purkinje fibers and ventricles. All sets stage for reentry in
ventricles. Reverse arrhythmias by adm of K salts, phenytoin or lidocaine. If lifethreatening, give anti-digitalis Ab to neutralize the drug.
 CNS: CTZ stim  vomiting. Diarrhea from activation of dorsal motor n. of vagus
 GI motility. Also anorexia, lethargy and fatigue, visual problems (hazy vision,
disturbed color perception, photophobia), dizziness and headache.
 Vasculature: vasoconstr of art and veins b/c  intracellular Ca in sm m cells.
Coronary arterioconstr MI
 Skeletal m: Fatigue and muscle weakness b/c electrolyte imbalance.
 Predisposing factors = hypokalemia (by diuretic)  digitalis binding;
hypercalcemia  extrasystoles. Impaired renal (digoxin) (quinidine competes w/
clearance) and hepatic (digitoxin) fcn. Hypothyroidism ( t1/2 of digitalis via 
renal clearance of drug (digoxin)
 Drug interxn: 1 blockers and antiAchE, adrenolytic, same fxs. Worst combo =
use w/ Ca entry blockers (verapamil) b/c  contr + cond vel.
Drug of choice. 12-hydroxy digitoxin. Polar and no plasma prot binding or hepatic
metabolism. Elim unchanged by kidney. T1/2 = 40 hr  tissue accumulation.
lipophilic  extensive plasma prot binding and hepatic met. Easily displaced by other
plasma prot binding drugs. Renal elim of polar metabolites. T1/2 = 5-7 days  more
tissue accumulation.
short term i.v. therapy of severe refractory CHF.  CO and  PVR. Inh PDE, just like
methylxanthines. Toxicity and  myocard oxygen demand.
amrinone analog. More potent, less toxic, given p.o.
short term management of severe refractory CHF, sxs of acute CHF in cardiogenic
shock.  1 stim  potentially dangerous.
Cardiac Arrhythmias
antiarrh drugs suppress abnormal automaticity and cond in depolarized cells, but
Class I (IA, IB, & IC)
Class IA
quinidine
procainamide
disopyramide
Class IB
lidocaine
Tocainide
mexiletine
phenytoin
Class IC
minimally affecting activity in normally polarized regions of the heart. @ hi doses, 
cond in normal tissue  drug induced arrhythmias.
Cond. Vel fcn of phase 0 dp/dt and amplitude.
Na channel blockers.  upstroke and amplitude of AP   cond vel 1’ in injured tissue
and prolong ERP and AP of both normal (?) and injured Purkinje fibers and cardiac
muscle.
Na channels blocked in activated state by binding to h gate. Depr of ectopic
pacemaker rate, cond vel , prolong ERP. Prolong AP by partial blockade of K channels
w/ in repolarizing outward current.
Most common p.o. antiarr drug. Completely absorbed after p.o.,  bound to plasma
prot. Partial hepatic met and partial elim by kidney unchanged.
Cardiac toxicity: antimusc   HR and  cond in AV node. E.g. use quinidine in
presence of atrial flutter   vent rate  v. tach   CO syncope. Lo dose of
digitalis (vagomimetic) given b/f quinidine counteracts antimusc axn. Also can give
diltiazem to  cond @ AV node. Hi dose  AV block and  contr  cardiac arrest.
Asystole in pts w/ depr SA node.
Extracardiac toxicity: 1 R block  vasodil  hypotension and reflex tachy. Also GI
distress and cinchonism (CNS-mediated headaches, dizziness, and tinnitus).
Thrombocytopenia rare.
Contrax: AV block, severe hypotension, hyperkalemia, digitalis toxicity, M.G. (can
aggravate it b/c partial NMJ blocker)
Tx: Works best in ischemia. Mainly atrial and some ventr. arrhythmias. E.g. premature
atrial contr, paroxysmal atrial flutter and fibrillat’n, reentrant arrhy, WolffParkinson/White tachy, and v. tachy.
Drug interxn:  digoxin blood levels by  renal elim. Hi dose potentiate  blockers. 
action of coumarin anticoagulants.
drug of 2nd choice after lidocaine for v. arrhyth. Less intense fx than quinidine.
Cardiac toxicity: Less atrial and v tach, and hi doses cause SA and AV depr b/c less
antimusc. Extracardiac tox: Ganglionic blocking activity  hypotension, neg
inotropic fx,  CO. SLE, skin rash, hepatitis, and GI distress.
p.o but NOT bound to plasma prot. Hepatic met to N-acetylprocainamide (active
metabolite)  accumulation = toxicity. Parent and met. both elim by kidney. Contraind
similar to quinidine
drug of 2nd line for v. arrhyth. in pts who can’t tol either quinidine or procainamide.
MORE antimusc (atropine like sxs) and neg inotropic actions than quinidine. P.o. and
highly plasma prot bound. Long duration of axn and hepatic met is active. Contraind
similar to quinidine but also in glaucoma.
Na ch blockers in both activated and inactivated states for ventricle disturbances, no
fx on nodal or cond tissue. Mech unkown.  AP duration and prolong diastole. Works
on depolarized tissue (ischemia, dig tox), not on normal tissue (atrial flutter and fib). NO
antichol.
1st choice for v tach and prevent of v fib after acute MI. Also for E disturbances of dig
tox. Extensive 1st pass & hence p.o. Metabolites less active but could accumulate. NO
cardiac tox = safest antiarr drug. . Extracard tox: CNS toxicity, paresthesias, tremor,
convulsions, nausea, and drowsiness. Contraind in pts w/ 2 nd or 3rd degree block b/c
blocks idiovent pacemaker.
struc analogs of lidocaine. Resistant to 1st pass hepatic metabolism. Can be p.o. but
need hi doses. Similar to lidocaine in all aspects. Also cause blood dyscrasias, e.g.
leukopenia, agranulocytosis and thrombocytopenia.
anticonvulsant w/ limited antiarrh prop. 2nd line drug. Similar but less fs as
lidocained. Tx E disturbances assoc w/ dig tox. Block both Na ch and slow inward Ca
current (depolarization) evoked by dig (?).
Potent Na ch blockers for v arrhyth.  phase 0 AP   cond vel w/o fx on ERP or
AP in Purkinje fibers. Suppress premature ventricular contr and  v. response to atrial
flecainide
Class II
Class III
bretylium
amiodarone
sotalol
Class IV
flutter or fib. SE: CNS related dizziness and blurred vision
marked  cond vel, CNS: numbness in finger and feet.
 1 R blockers, esp in nodes automaticity. Prolong AP/ERP, no  in cond vel.
Indirectly  Ca influx. Tx sinus tach caused by anxiety or thyrotoxicosis or
pheochromocytoma; v tach during atrial flutter or fib; dig induced arrhy; PAT. Contraind
in pts w/ CHF, dig tox (?) asthma
prolong AP/ERP in ventricle w/o altering phase 0 depol/memb pot.  strength of E
stim needed for v fib. Also for intractable (when fails to respond to other drugs) v tach
and controlling fib.
emergency tx of intractable v tach
Tx PAT and v arrhyth. Ca >>Na blocker   sinus rate and AV nodal cond. Must 
dose to  SE: hypotension, neg inotropy, photosensitivity, corneal deposits, pulm fibrosis,
hepatic necrosis, affect thyroid fcn b/c releases iodide from drug and long t1/2 = 3-4 mos
b/c  Vd, accum in fatty tissues.
Like bretylium. In add’n, blocks  R.
Ca ch antag. Block slow inward Ca current during phase 0-4, esp in SA and AV nodes,
not in cardiac mscles.  cond vel and  ERP. Verapamil, diltiazem and bepridil. Tx
reentrant supravent tachy and PAT by converting atrial flutter or fib to normal rhythm.
SE: neg inotropic, contraind in pts w/ CHF, or taking  blockers. Hypotension b/c
vasodil assoc w/ diltiazem.
Cancer Chemotherapy
alkylating agents
nitrogen mustard der.
Mechlorethamine*
(HN2)
chlorambucil
melphalan (L-PAM)
cyclophosphamide*
(CYC)
ifosfamide (w/mesna)
busulfan
nitroureas
Carmustine* (BCNU)
lomustine* (CCNU)
semustine (methyl
CCNU)
streptozocin (antibiot)
alkyl sulfonates
busulfan (Myleran)
ethylenimines
trethylenethiophosphor
amide (thiotepa)
triazenes
dacarbazine *(DTIC)
Radiomimetics. Methyl gp on N highly reactive and alkylate G @ N-7. Resistance by
DNA repair enz. Vesicant or highly irritating action on skin if extravasation should occur
during i.v.
must be i.v. b/c so reactive. Alkylat’n of DNA by ethylenimonium ion (interstrand xlinking). Rapid inactivation. GI, BM, alopecia, extravasation. Tx Hodgkin’s dz.
p.o
p.o.
very stable. i.v. /p.o. Biotransformation required @ liver to acrolein (F.R., combined
w/N-cysteine, a FR scavenger) and phosphoramide mustard (p.m.). P.m is the active anticancer metabolite. SE: GI, BM, hemorragic cystitis (developed in 30% of pts. @ hi
dose  acrolein toxicity, bladder, ureter + renal pelvis, hemauria prevented by mesna),
alopecia. Tx: lymphomas, breast ca…
ifosfamide analog of CYC. mesna a potent FR scavenger to prevent hemorrhagic cystitis.
BM, CNS, renal failure, even more hem cystitis. Tx testicular ca, sarcomas.
unique toxicity = interstitial pulm fibrosis, also severe BM suppression.
toxic against brain tumors and lymphomas, b/c lipophilic and XBBB. Delayed marrow
toxicity. BM tox last longer (4-6 wks) than by other alkylating agents (2-3 wks).
SE: Addisonian like, BM fibrosis,  blood count,  dosage for BM transplant b/c
profound BM suppression. Tx: chronic myelogenous leukemia (CML)
Sim to N mustard, but more stable. Toxicity similar.
nonclassical alkylator that causes formation of DNA adducts. Also an anti-metabolite
procarbazine*
platinum
cisplatin *(DDP)
Carboplatin
(paraplatin)
antibiotics
anthracyclines
doxorubicin*
(adrimycin)
Daunorubicin*
(cerubidine)
idarubicin*
bleomycin*
Miscellaneous
dactinomycin*
Plicamycin
(mithramycin)
mitomycin
streptozocin*
mitoxantrone
Plant derivatives
vinca alkaloids
vincristine*
Vinblastine*
b/c a purine. Light sensitive; N-demethylation by p450  toxic (alkylates DNA) once
converted. SE: principal tox on GI (nausea and vomiting), little BM suppression. Good
drugs to combine with other drugs that cause serious BM. Tx: Hodgkin’s dz; melanoma.
highly reactive oxygen radicals  degradation of DNA. XBBB.  xsomal breakage
 mutagenic, teratogenic, and carcinogenic. Used 1’ in MOPP rgimen for Hodgkin’s.
SE = GI and BM. CNS tox (sedation and depr) and skin rashes, esp @ hi doses. Only
cancer drug that has disulfiram rxn. Also a MAO inhibitor.
Given @ set dose based on renal toxicity. Tx: In combo therpay for esp metastatic
testicular ca, also germ cell ovarian ca and small cell lung ca. Cis Cl is the active form
that binds to DNA at nucleophilic sites intrastrand DNA x-link on G’s. Unionized in
extracellular space b/c Cl rich. Becomes unionized in Cl depleted cell. Not phase specific
and highly bound to proteins. Renal clearance  can cause renal failure (dose related
and cumulative), so must give w/mannitol for diuresis. SE also includes ototoxicity,
neurotox (peripheral neuropathies—tingling, numbness), severe emesis (tx w/ 5 HT3
antag, Ondansetron); mild BM.
Given @ higher dose than cisplatin. Mech the same, but rate of active metabolite
generation slower  longer plasma t1/2. More BM, rare nausea. Less renal tox. Not for
curative intent. Tx: ovarian ca, lung ca.
Mech: interaclation  steric hindrance  interfere w/ DNA synth.. Topo II inh. Also
Metal ion chelation; FR formation Extensive biotransformat’n in liver. SE: vesicant upon
extravasation. BM, severe alopecia, GI, cardiac damage b/c sensitive to FR. Give w/
FR scavenger to  cardiac tox, but may  anti-cancer fx. Cardiac toxicity (damage to
myofibrils  CHF) dose related. Given < 500 mg/m body surface for life time.
Exacerbated by exposure to alkylating agent, radiation therapy, radiation recall (drug
given after radiation). Tx: malignant lymphomas, breast ca, sarcomas
tx leukemia
bifunctional w/ DNA binding and active redox sites. In the absence of Fe3+ and O2 
no damage. In the presence, Fe2+ releases electron to DNA  covalent binding. Renal
clearance. SE: bleomycin hydrolase = degrad enz absent in lung and skin  pulm
fibrosis. Most toxic drug to lung. Also skin rash, esp in fingers. Also get
anaphylaxis/hypersensitivity. Not much BM
@ hi dose, inh DNA, @ lo dose, inh RNA. Tx Wilms’ tumor.
Tx hypercalcemia. Toxicity to bone by inh bone formation
hemolytic uremia syndrome (kidney damage and  platelets b/c consumption of platelets)
an antibiotic but acts like nitrosoureas. Tx insulinoma b/c causes Islet cell damage.
Otherwise,  cell tox = SE  DM in pts
similar to doxorubicin, but less cardiotox.
work just like cochicine excpet much more potent  v. toxic
microtubule damage, mainly in nervous system  metaphasal arrest and inh axonal
transport. Hepatic clearance. Peak short lasting though prolong terminal plasma t1/2 =
long tail  accumulation in nerve. SE: neurotoxic; extravasation. Tx ALL, less so for
lymphomas.
microtubule damage mainly in myeloid cells of BM. Short terminal t1/2 and no long tail
(conc x T= exposure of rapidly dividing cells to drug). BM, neurotox rare. Tx germ cell
tumors; lymphomas; breast ca.
Vinorelbine
(Navelbine)
epipodophyllotoxins
etoposide (VP-16)
Teniposide (VM-26)
Yew tree der
paclitaxel (taxol)
taxotere
Camptothecin der
(irinotecan [CPT 11])
antimetabolites
Methotrexate*
5-fluorouracil (5-FU)*
floxuridine (FUDR)*
Cytarabine* (cytosine
arabinoside; ara-C)
purine analog*
6-mercaptopurine *
(6-MP)
Allopurinol*
Complexing w/Topo II SS breakage of DNA. Phase specific (S and G2). Schedule
dependent (given 3-5/d, to  chance of hitting ca cells during specific phases of cell
cycle); hepatic biotransformation; renal clearance. SE: BM, GI, alopecia, vesicant action
at site of injection, vasomortor hypersensitivity, neuropathy. Tx: refractory testicular ca;
small cell lung ca.
New drug under developmenttx children’s tumor.
Given w/ cremifor (caastor oil), i.v. 3-24 hr infusion. Large Vd. Hepatic metabolism and
nonrenal clearance. Promotes assembly of microtubule and stabilizes them  abnormal
arrays of microtubules thruout cell cycle  apoptosis. SE: BM (dose limiting),
hypersensitivity, hypotension or bradycardia, peripheral neuropathy, arthralgia/myalgia,
severe alopecia, occasional hepatic dysfcn. Tx: ovarian ca (in relapse), breast ca.
mech same as paclitaxel. Water soluble, 1-hr infusions (w/o cremifor). SE: skin rashes,
effusions and endothelial damage  edema, tx w/ corticosteroids; rare hypersensitivity.
BM. Alopecia. Tx same as above.
Topo I inh (during SS cleavage, binds to strand (?), prevent DNA reannealing and stop
repl fork. Prodrug w/ complex biotransformat’ns, schedule dependent. SE: BM,
diarrhea, nausea, vomiting, mucosistis, alopecia. Only tx for fluoropyrimidine resistant
colorectal ca.
inh active site of enz or allosteric site., or act as false substrate.
folic acid analog. Inh dihydrofolate reductase. Can directly be injected into CSF since
does not xBBB. But can leak into systemic circ. So give leucovorcin (N-formyl FH4) to
prevent BM suppression. Also, @ hi dose of MTX, it can bypass carrier and go into the
cell. Then give leucovorin which rescues normal cells preferentially b/c they can conc
leucovorin better. This way, get selective killing of cancer cells. Renal exc’n, so need
good renal fcn. Monitor blood level of MTX. SE: BM; GI, liver dysfcn; mucositis.
Efficacy: IT (?)leukemia, mg/m2 head and neck, choriocarcinoma, breast. gm/m2,
osteosarcoma adjuvant, childhood ALL.
pyrimidine analog. curative in early stage and palliative when advanced. Inh
thymidylate synthetase , which forms 4’ complex w/ leucovorin @ hi dose of
leucovorinenhance 5-FU). Extensive metabolism. 5-FdUMP=active metabolite. SE:
BM (bolus), GI (cont infusion or w/ leucovorin  mucositis/diarrhea). Tx: advanced
colon ca (for stage 3, 5-FU 1/3 cure rate improvement after lymph node resection), breaast
ca.
complete 1st pass if given via hepatic artery. SE: cholangitis. Tx: colon ca metastic to
liver.
pyrimidine analog competitive inh DNA pol in S phase. Inh also DNA repair. Forms
defective DNA. Must give 2x/d for 5-7 days to gets cells sensitive. Biotransformat’n,
including intracellular. Schedule dep. must be given continuously e.g. 2-wk cont
infusion. SE: BM, GI, @ high dose cause neurotox. Mucositis. Tx Acute myelogenous
leukemia
6-thioguanine, acts as false precursor. Not degraded by xanthine oxidase. No drug
interxn w/ allopurinol. Can only be a maintenance therapy for low tumor burden if used
w/o allopurinol. BM. Tx acute leukemia.
Purine analog. inh purine ring synth by inh several enz systems, and acting as false
precursor. Similar to Imuran. Normally degraded by xanthine oxidase, so must give hi
dose. If given w/allopurinol, must  dose. SE: BM; liver damage. Tx acute leukemia
(childhood ALL)
a supportive agent, not an anticancer drug by itself. Xanthine oxidase inhibitor. Pts w/
large tumor masses or extensive met ca metab lots of purines from malignant cells into
uric acid via xanthine oxidase. Allopurinol prevents uric acid nephropathy.
Purine nucleoside
analogues
fludarabine
deoxycoformycin
2chlorodeoxyadenosine
miscellaneous
hydroxyurea
Hormones + hormone
antagonists
diethylstilbestrol (DES)
tamoxifen*
Prednisone*
dexamethasone
Megestrol acetate or
Megace
androgens
flutamide
Leuprolide,
goserelin/Zoladex
aminoglutethimide
Octreotide acetate
sandostatin
miscellaneous
procarbazine
(Matulane)
Mitotane (o,p-DDD)
Not need to know. Yay!
L-Asparaginase*
Estramustine
phosphate
levamisole
all requires intracellular activation and inh intracell enz. BM. Tx chronic lymphocytic
leukemia.
inh ribonucleotide reductase and DNA  pol.
inh adenosine deaminase
causes DNA strand breaks and apoptosis. Tx hairy cell leukemia.
replaces usulfam for CML. Also for essential thrombocythemia.  fetal Hb exp’n in
sickle cell anemia pts. Mech: Inh ribonucleotide reductase. Well absorbed orally. BM
(rapidly reversible).
Tx prostate (b/c suppress androgen synth), also breast ca (?)
synthetic nonsteroidal mixed antagonist/agonist on estrogen Receptor. Hepatic
biotransformation.  t1/2. SE: flushing, leukopenia and rare hypercalcemia, hot
flashes, vaginal dryness or discharge.. Tx: breast ca by directly inh growth of ca cells
w/R, but no effect on cells w/o R. (Estrogenic effect improves cardiac and osteoporosis
risks. But estrogen also a carcinogen b/c see small  in endometrial ca. Try to elim
estrog fx by designing anti-estrog drugs. NONE available.
glucocorticoids. Used in MOPP and other combo. SE: hi dose  feeling of well being
 prompt weak pt to overexert. Prednisone short t1/2, and dexa long t1/2. Tx ALL,
lymphomas,  toxicity of chemo.
progestins, Tx endometrial ca. 2nd line therapy for breast ca. Used in HIV pts to stim
appetite (prevent wasting).
Used occasionally for breast ca
antiandrogens. For prostate ca.
LHRH and GNRH agonists  downreg of R @ the pituitary  medical castration.
Effect of initial testosterone surge blocked by antiandrogens.
aromitase inhibitors. For females who converts peripheral androgen to estrogen, can use
this drug to block the conversion.
somatostatin analogue. T1/2 = min. Maintains GI mobility, for pts w/ diarrhea. S.C.
injection for symptomatic tx of carcinoid syndrome (malignant, seen in ileum/stomach,
bronchus, somtimes testes/ovary. Carcinoid prod 5-HT (tricuspid
fibrosisinsufficiency), bradykinin  severe flushing and diarrhea.
nonclassical monofunctional alkylator. XBBB. SE: GI, BM, disulfiram/antabuse like
rxn, neurotoxic,  pyridoxal phosphate, MAO inh, allergy, skin rashes, most potent
carcinogen and causes  delayed carcinoma. Classic drug in combo therapy for
Hodgkin’s dz.
DDt relative. Conc in adrenal cx. Adrenocortical necrosis  palliation of inoperable
adrenocortical adenocarcinomas. Must be given w/ adrenal replacement. SE: skin rashes;
encephalopathy, anorexia, nausea, diarrhea, lethargy, dizziness.
Large bacterial protein given IM/IV. Acts extracellular (EC) to depletes tissue Lasparagine. Deaminates EC L-asparagine to aspartic acid inh protein synth and
apoptosis. Asn usu a nonessential AA. But essential in ca cells b/c they lose asparagine
synthetase. Therefore this targets sensitive cells but also select for cells that can produce
synthetase. Only produce remission for a brief period, but must be combined w/cytosine
roboside and antibiotics. SE: anaphylaxis;  serum proteins, pancreatitis,
encephalopathy, clotting factor abnormalities, ammonia toxicity in CNS. Tx acute
lymphoblastic leukemia.
combines alkylating agent w/hormone  localization of alkylating agent at hormonally
responsive tumor site. Minimally useful for prostate ca.
immunomodulation and deworming agent in animals. Allergic rxns, blood count depr.
Hepatic lesions mimics metastatic ca. Used as adjuvant therapy for colon ca (w/ 5-FU)
all-trans-retinoic acid
Investigational. induction of cell differentiation. SE: skin cracking, headache,  blood
cholesterol and TG,  WBC and platelet, liver tox, cardioplulm distress. Tx
promyelocytic leukemia.
Antimicrobials
Abbreviations used in this section:
R = resistance p.o.= absorbed well orally
X-sensitivity = cross sensitivity
X-R = cross resistance
Def= deficiency
Met = metabolism
 Vd = distrib well throughout tissues
 = lots/long/many
Folate Antagonists
sulfonamides
sulfasalazine
Sulfadiazine*
sulfisoxazole
sulfamethoxazole*
sulfacetamide
trimethorprim
Co-trimoxazole
Mech: inh synthesis of FH4  inh formation of purines, pyrimidines, and certain AA 
bacteriostatic. No longer drugs of choice for UTI’s b/c of SE and R. Plasma prot
binding. Hepatic met. Renal elim. SE: Metabolites ppt at acidic pH  crystalluria, need
adequate fluid intake and alkalinization of urine. Hypersensitivity. Hematopoietic:
agranulocytosis, megaloblastic anemia, aplastic anemia, hemolytic anemia and
thrombocytopenia uncommon. Hemolytic anemia* in pts w/ G-6-PD deficiency.
Kernicterus in newborns b/c displace bilirubin from albumin  bilirubin XBBB  irrev.
brain damage. Adverse Drug Interxn: potentiation of sulfonylurea hypoglycemic drugs,
orgal anticoag, phenytoin, and MTX via prot binding or competition for hepatic metab
and renal sec’n.
not well absorbed p.o  tx Infl Bowel dz, e.g. Crohn’s dz and ulcerative colitis.
worst crystalluria. Used in combo therapy. Metabolite 5-aminosalicylate works just like
aspirin = anti-infl. W/ pyrimethamine to tx malaria. Conc best in CSF and brain.
least likely to cause crystalluria. Most useful when used alone
least likely to cause crystalluria. Used in combo therapy.
topically for eye infections
competitive inh of dihydrofolate reductase  inh FH2 going to FH4. Low affinity to
mammalian enz. Bactericidal. Lipophilic   Vd. SE: No rashes or other
hypersensitivity. GI distress. Folate def  BM. Tx OD by giving FH2 and/or FH4.
trimethoprim + sulfamethoxazole. Synergistic. Sulfonamide  FH2 formed  FH2 to
compete w/ trimethoprim for dehydrofolate reductase. Combo bactericidal.  SE since
 dose. SE: hypersensitivity and GI distress. Tx UTIs, resp, GI and gonorreha
infections, and PCP and isospora belli (diarrhea) in AIDS pts. Also uncomplicated UTIs
and prostatitis caused by Enterobacteriaceae, orchitis and epididymitis caused by
susceptible bacteria and chalamydiae.
Inhibitors of cell wall synthesis
Pencillcins
Bactericidal, against rapidly dividing bacteria that synth a peptidoglycan cell wall.
Synergistic w/ aminoglycoside antibiotics. Forms covalent bond w/transpeptidase
weakened cell wall. Murein hydrolases (autolysins) which normally remodels cell wall
continue to work cell lysis.
Incompletely absorbed p.o. alter intestinal flora  tx salmonella derived enteritis.
Vd but no bone/CSF unless these areas infl.  bind to plsma prot (> 90%).
Tubular sec’n (90%). Probenecid inh sec’n   plasma levels.  dose in pts w/
impaired renal fcn.
SE:





Natural penicillins
penicllin G (benzylpcn)
procaine pcn G
benzathine pcn G
penicillin V
(phenoxymethylpcn)
Antistaphylococcal pcn
vancomycin
ciproflxacin
rifampin
imipenem/cilastatin
Extended spectrum pcn
ampicillin
amoxicillin
Clavulanic acid
sulbactam
tazobactam
Antipseudomonal pcn
azlocillin
mezlocillin
piperacillin
ticarcillin or
carbenicillin +
clavulanic acid
hypersensitivity in 5% of pts: hepatic met to penicilloic acid  haptenized 
urticaria, angioedema, and anaphylaxis. X-sensitivity.
Diarrhea**: altered intentinal flora   C. difficile peudomembranous colitis
from toxin.
Neurotoxicity: seizures upon intrathecal injection esp in pts w/ epilepsy.
Platelet dysfunction** inh platelet aggr by carbenicillin and ticarcillin (binding to
ADP R). CI in pts predisposed to hemorrhage.
cation toxicity: carboxy pcn adm as salts. Should use a more potent pcn to avoid this
problem.
For G+ and G- cocci, G+ bacilli and spirochetes. Unstable in stomach must be i.m.
Pcn G salts in i.m repository.
More acid stable  better than Pcn G for p.o. V&G inactiv by -lactamases. Less
effective than Pcn G against G- (Neisseria and Haemophilus and some anaerobic species),
NOT effective against aerobic G- enterobacteriaceae and Pseudomonias. Tx strep,
penumoncoccal, anaerobic(except B. fragilis), gonococcal infections, syphilis.
used for methicillin resistant staphylococci only.
less potenet than Pcn G against G+ and G- cocci. Drugs of choice for G+ bacillus,
Listeria monocytogenes. Also for G- bacilli & G- Enterobacteriaceae. Tx URTI
caused by Haemophilus, and also uncomplicated UTI.
not well absorbed p.o. GI distress, overgrowth of other organism, and  diarrhea. SE:
rash (maculopapular) occurs most frequently w/ampicillin.
completely absorbed from GI  no diarrhea and no altering intestinal flora.
penicillinase inhibitor. Used with ampicillin and amoxicillin.
effective against many G- bacilli including P. aeruginosa and enterobacteriaceae. NOT
effective against klebsiella b/c consitutive -lactamase present.
most potent of the group
adm i.v. b/c not absorbed p.o, inh platelet aggr, also adm as Na or K salt hyperkalemia
and hypernatremia. Tx klebsiella
Cephalosporins
1st gen
cefazolin
2nd gen
struct, fcn, mech just like pcn’s. More resistant to -lactamases. Unstable in stomach 
i.v. Renal elim and little hepatic metab, except for cefoperazone and ceftriaxone
(hepatobiliary route). Hypersensitivity common but less freq. 15% x-sensitivity w/ pcn
so CI in pts sensitive to pcn.
R to staph penicillinase. Against G-, e.g. Proteus mirabilis, E. coli, and Klebsiella
pneumoniae (PEcK). Good acitivity against G+ and moderate activity against G-. Tx
UTIs, resp and skin infections.
most popular iv. surgical prophylaxis.
Less active than 1st gen against G+, but  activity against G-. Also inh H. influ,
Enterobacter aerogenes, and Neisseria (HENPEcK). Do not inh Psudomonas species or
bacteroides except for cefoxitin, which tx B. fragilis. Tx UTIs, resp infections, aspiration
cefotetan
3rd gen
cefixime
Cefotaxime
cefamandole
cefoperazone
pneumonitis, intraabdominal and pelvic infections.
tx intraabdominal and pelvic infections b/c activity against most enterobacteriaceae and
anaerobic species.
Little activity against G+ (cocci), but superior activity against G- bacilli. Spectrum =
Those of 2nd gen plus Pseudomonoas aeruginosa and Serratia marcescens. Tx
nosocomial resp infections, UTIs, skin struct infections, osteomyelitis.
only drug given p.o., Tx Haempophilus and gonorreha.
drug of choice for meningitis caused by H. influenza (most lipophilic b/c XBBB).
Disulfram like rxn  don’t drink. Also inh formation of vit-K depedent clotting factors
 bleeding. Don’t give w/ aspirin, dicoumarol/warfarin.
Other -lactam antibiotics
carbapenems
imipenem
+ cilastatin
Monobactams
aztreonam
synthetic -lactam. Broadest spectrum -lactam. Active against penicillinase-producing
G+ and G-, anaerobes, and P.aeruginosa. But R in P. aeruginosa begin to appear. Renal
elim and No hepatic metabolism. XBBB. O.D. seizures. SE: hypersensitivity & Xsensitivity to pcn. Adm i.v. Rapid i.v. infusion  nausea and vomiting. Extensive
hydrolysis in kidney  metabolites nephrotoxic, &  [parent drug]  effectiveness in
treating UTIs. Must be given w/cilastatin, an inhibitor of renal dihydropeptidase.
Together tx serious infection of unknown origin.
very narrow spectrum but R to -lactamases. Inh only aerobic G-, mainly
enterobacteriaceae and P. aeruginosa. Tx bacteremia, UTIs, resp infections,
osteomyelities and skin struc infections. i.v./i.m.. Renal elim unchanged. V.safe. No
hypersensitivity. Good substitute for Pcn in pts allergic to Pcn and have G- infection.
Non -lactams but inh bact cell wall synthesis
vancomycin
bacitracin
Inh cell wall synth by binding to free COOH of D-Ala (end of pentapeptide), interfere w/
elongat’n of peptidoglycan backbone. Inh only G+, b/c its MW and can’t X OM of
G-. Bactericidal against G+ cocci and bacillli, e.g. staph and strep. Bacteriostatic
against enterococci (faecalis and faecium). W/aminoglycoside =synergistic/ bactericidal.
Not absorbed p.o. tx pseudomemb colitis caused by C. difficile or staph in colon.
Only for serious infections, mainly staph in pcn allergic pts and methicilliln R staph.
Also prophylaxis to prevent endocarditis in pts w/ valvular heart dz undergoing
dental/surgical procedures.
SE:
w/aminoglycosides   ototocity that occurs @ hi doses, also nephrotoxicity.
Phlebitis caused by i.v., prevented by adm of diluted sol’n.
Older prep impure  red man syndrome = head and neck erythema and hypotension b/c
extensive histamine release.
mixture of polypeptides that inh cell wall synth. Bactericidal against a wide variety of
G+. Topical, not systemic b/c of its nephrotoxicity. Combined w/ neomycin
(aminoglycoside) and/or polymyxin (a detergent that breaks OM of G-)
Inhibitors of prot synthesis
Tetracyclines
Mech: Entry into G+ E dependent, G- by diffusion thru porins of OM  into cytoplasm
thru prot-carrier. Binds to 30S ribosomes. Weakly bound to ribosomal prot. R via drug
efflux prot induced by drug + mutations in OM prot.
Broad-spectrum. But widespread resistance limit its use.
Drugs of 1st choice Mycoplasma pneumoniae, chlamydial infect’n affecting sexual
organs, syphilis if on long therapy. No longer used for N. gonorrhoeae, or UTIs.
P’kinetics:
 absorption: Dairy foods, Mg/Al antacids, Fe prep  GI absorption if given p.o. b/c
chelates w/ cations.
 Distribution: bind to calcifying tissues, e.g. teeth and bones. Partial hepatic met
(glucuronidat’n) and partial renal elim unchanged. CI in pts w/ renal dysfcn except
when using doxycycline. All X placenta and conc in fetal bones and tooth.
For the 2 drugs below
Minocycline
doxycycline
SE:
 GI—irritation of gastric mucosa, controlled by co-adm of foods other than dairy
products.
 Deposition in bone and 1’ dentition during calcificati’n during growth 
discorloration and hypoplasia of teeth and temporary stunting of growth. Avoid use
in pregnancy and children under 8.
 Fatal hepatotoxicity—in pregnant women w/ pyelonephritis.
 Phototoxicity: severe sunburn if exposed to sunlight only for a short period. Worst =
doxycycline and demeclocycline.
 Suerinfections: get candida in vagina or resistant staph in intestine.
V. lipophilic  enter G- thru OM and porins, less affected by drug resistance, escapes
chelate formation  absorbed the best . Bacteriostatic. Tx rickettsial dz such as Rocky
Mt Spotted Fever and typhus
prophylactic to eradicate carrier state of meningococci b/c XBBB best w/o infl. But
rifampin = preferred drug. SE: Ototoxicity  vestibular problems: dizziness, nausea,
vomiting b/c it conc in endolymph of ear.
prevent traveler’s diarrhea, but worst phototoxicity and R limit use, not
recommended. Used w/ H blockers for ulcers. Complete biliary exc’n, used in pts w/
renal dysfcn.
Aminoglycosides
amikacin
Tx serious infections due to aerobic G- bacilli, 1’ against Enterobacteriaceae /P.
aeruginosa, Staph and strep inh. Tx endocarditis from enterococci or viridans strep but
must be adm w/ pcn. Gentamicin preferred b/c streptomycin R common. Bactericidal
against only aerobic, but not anerobic bacteria.
Transport thru bact cell wall and cyto memb. Not need to know transport:
assoc b/t cationic drug and anionic surface  penetration thru pores of OM of Gbacteria, or disrupt OM & uptake thru nonporin ch, or water filled areas of peptidoglycan
wall in G+. Then binds to transport molecule in ETC  moves X memb, oxygen
dependent  binds to 30S  polysome disaggr to monosomes and misread mRNA
Transport inh by divalent cations.
Resistance via
  uptake b/c oxygen dependent transport is altered
 30S binding site  affinity.
 Enz modification of aminoglycoside plasmid mediated   drug affinity for 30S
not accum w/n bact.
P’kinetics:
 polar and polycationic  p.o. absorption, must be i.v. or i.m. NOT XBBB. Conc
most in renal cortex and endolymph/perilymph of inner ear  nephrotoxic/ototoxic. X
placenta and accum in fetal plasma and amniotic fluid.
No hepatic met b/c so polar already. Renal elim.  dose in pts w/ renal dysfcn/failure.
SE:
Nephrotoxicity -Rev (b/c renal tubular cells can regen) renal impairment in 5-25% of pts
on drug for > 3d. Trapped in lysosome and inh PI specific phospholipases  inh PG synth
 unopposed AT II vasoconstrict’n and inh glom filtration. Also inh sphingomyelinases
and ATPases and alter mito fcn and ribosomes in prox tubular cells.
Ototoxicity—vestibular (damages organ of Corti, esp outer hair cell in basal
turn)/cochlear (hair cells of ampullar cristae) directly related to peak plasma level and
duration of tx.
NMJ block—in pts w/ MG and pts undergoing surgery on anesthetic and NMJ blockers.
By inh presynaptic release of Ach and postsynaptic R blockade.
resistance develops least to it. More auditory toxicity. So does kanamycin.
neomycin
streptomycin
must be topical b/c most severe nephrotoxicity.
least nephrotoxic. More vestibular toxicity. So does gentamicin
Erythromycin—macrolide antibiotic
broad spectrum same as Pcn G, bacteriostatic. Bind to 50S. R via  uptake and 
affinity for 50S. P’kinetics:  Vd, enhanced by infl, except no XBBB. Accum in
prostatic fluids and Mphages and liver. Metabolism: extensive p450, then renal elim.
Active drug goes thru enterohepatic circulation.
SE: epigastric distress poor patient compliance. Cholestatic jaundice b/c
hypersensitivity. Transient deafness @ high doses. CI in pts w/ hepatic dysfcn b/c accum
in liver. Adverse Drug interxn (not need to mem): inh met of theophylline,
cyclosporine, carbamazepine, corticosteroids, and digitoxin. Fatal common combo =
terfenadine/astemizide + erythromycin @ hi dose  fatal arrhythmia “torsades de
pointes”.
Azithromycin
clarithromycin
troleandomycin
Chloramphenicol
chloramphenicol
Not widely used. Broad spectrum against bact and nonbact, esp for B. fragilis. but
limited to life-threating infections b/c its toxicity. Generally bacteriostatic but can be
bactericidal against certain org. Tx rickettsial dz if pt can’t tol tetracycline. Do not use
for UTI, resp or brucellosis infections b/c other less toxic drugs available.
Mech similar to erythromycin. Resistance via an R factor for acetyl co-enz A transferase
 inactivates drug. Also by  permeability.
p.o, also given i.v.  Vd b/c lipophilic (pleural, axcites and abscess fluids. XBBB and
other organs). Hepatic met (to glucuronide) and renal elim.
SE:
hemolytic anemias in pts w/G-6-PD deficiency. (sim to tox. of primaquine,
sulfonadmide). Rare, aplastic anemia as idiosyncratic rxn and usu fatal. Also more
common rev anemia.
Gray Baby Syndrome: in neonates b/c lo hepatic and renal fcn  drug accum   mito
ribosome fcn  cyanosis, usu fatal.
Adverse drug interxn: Inh P450 met of phenytoin, tolbutamide, chlorpropamide, and
dicumarol.
Clindamycin
Mech and R similar to erythromycin. X-R not a problem. Inh most G+ cocci and
many anaerobes but not aerobic G-. Most enterococci are R but actinomyces are inh.
Used 1’ for intraabdominal and gyn infections caused by anaerobic bact such as B.
fragilis. Alternative to pcn.
P’kinetics:
p.o.  Vd except no XBBB. Good entry into bone. Extensive met in liver (CI in pts w/
hepatic dysfcn) and renal elim. Some exc’n by bile and feces.
SE:
Allergic skin rashes. 3-5% of pts on clindamycin develop pseudomemb colitis b/c
overgrowth of C. difficile. This tx by p.o. vancomycin.
Spectinomycin
binds to 30S, i.m. Drugs of 2nd choice for acute gnorrhea caused by penicillinase
producing Neisseria gonorrhoeae (usu tx 1st by ceftriaxone if pt not allergic to pcn
and cephalosporins), or by nonpencillianse producing org in pts allergic to pcn.
Quinolones.
Nalidixic acid
(prototype)
New fluoroquinolones
Norfloxacin*
Ciprofloxacin*
Sparfloxacin*
ofloxacin
enoxacin
lomefloxacin
levofloxacin
pefloxacin
All quinolones: Bind cations   p.o. absorption Renal exc’n.
tx recurrent UTIs. Inh Topo II and IV (DNA gyrase). No X R with other
antimicrobials. R assoc w/xsome, not plasmid. By mutation in Topo and  permeability.
Effective aginst most G- that cause UTIs. G+ are resistant.  Vd. Met to a more active
metabolite.
SE: nausea, vomiting, ab pain. Less common are urticaria, photosensitivity, and fever.
CNS: headache and visual disturbances rare.
for norfloxacin and ciproxacin: less freq emergence of resistant strains. Most
susceptible to resistance = P. aeruginosa and Strep pneumoniae b/c only marginally
sensitive.  Vd. SE: CNS mediated nausea, headache, and dizziness. Caution in pt w/
CNS disorders. Crystalluria @ hi doses. CI: pregnancy and children under 18 b/c
cartilage toxicity in immature animal occurs. All fluoroquinolones: hepatic inactivation.
P450 < that of erythromycin.
More potent than nalidixic acid, tx both G+ and G-. For complicated and uncompl.
UTIs and prostatis.
More potent than norfloxacin but similar spectrum. Every drug from ciprofloxacin on
tx many ststemic infections and multiple R bact, e.g. many enterobact and G- bacilli.
Both i.v. and p.o. Alternative to toxic drugs such as aminoglycosides or drugs that require
i.v. e.g. extended spectrum pcn and cephalosporins.
not metab by P450, renal elim ( dose in pts w/renal dysfcn)
Not need to memorize.
Antimycobacterial Drugs  Vd = can reach most tissue b/c need to reach caseous granuloma
chemotherapy of TB
isoniazid
rifampin
ethambutol
must use combo therapy to prevent R during the long duration of therapy, up to 2 yrs. 1 st
line drugs = isoniazid, rifampin, ehtambutol, pyrazinamide
inh synth of mycolic acids. R via no uptake. No X R. Bacteriostatic in stationary phase
and bactericidal in rapid division. Selective for TB and M. Kansasii. p.o. but  by Al
in antacids. Vd but [CNS] lower. Met by acetylation and hydrolysis.
SE: peripheral neuritis (paresthesia) most common in slow acetylators, from
pyridoxal deficiency. Isoniazid bind to pyridoxal  deriv no vit activity. Corrected by
pyridoxine (vit B6). X milk. Hepatotoxicity: most serious SE, 1% incidence, jaundice,
in fast acetylators. Idiosyncratic hepatotoxicity: if taking rifampin and alcohol @ same
time. Hypersensitivity = rashes and fever. Memory impairment and convulsions.
P450 met. e.g. inh phenytoin met  nystagmus and ataxia. Fast acetylators at risk.
inh DNA-dep RNA polymerase (Inh initiation but not elongat’n). Selective for
prokaryotes. R emerges rapidly via  enz affinity for drug  never give drug alone for
TB. Usu w/isoniazid.
Spectrum: Bactericidal for both IC and EC mycobacteria. For TB and leprosy,
prophylactic for meningitis in Neisseria meningitidis or H. influ. Inh most G+ bact such
as staph and strep, many enteric species (Pseudomonas, Legionella, mycoplasmata and
chlamydiae). Most anaerobic (C.difficile and B. fragilis)
P’kinetics: lipophilic, p.o. and  Vd, XBBB. P450 induction, observed the most. SE:
Nausea, vomiting, rash and fever. Hepatotoxicity rare.
bacteriostatic and selective for M. TB and M. kansasii. Used in combo w/ isoniazid,
rifampin and pyrazinamide for TB. CNS entry adequate for TB meningitis. SE: optic
neuritis   visual acuity and poor discrim b/t red and green (rev upon w/drawal).
Worsen gout b/c inh uric acid exc’n by kidney.
pyrazinamide
2nd line of drug for TB
ethionamide
cycloserine
Aminoglycosides
Chemo for leprosy
dapsone
clofazimine
p.o. bactericidal, Short Term initial therapy in combo w/ isoniazid and rifampin. 1-5%
on this combo get hepatotoxiity. Urate retention  precipitate acute attack of gout
struct analog of isoniazid but mech unknown. SE: GI distress and CNS: headache and
depr
 Vd. CNS: convulsions and exaggerated epileptic seizures, and peripheral
neuropathies.
streptomycin, kanamycin, and amikacin
dapsone + clofazimine + rifampin. Must be in combo b/c R can develop to any one drug
during the long duration of the tx.
related to sulfonamide, bacteriostatic by inh folate synth. p.o,  Vd, liver met. SE:
hemolytic anemia and methemoglobinemia via oxidation by hepatic metabolite. GI
distress, headache, peripheral neuropathies, psychoses, tinnitus, and skin rashes. Can
provoke lepra rxns, controlled by glucosteroids. Can tx PCP in AIDS pts.
bactericidal to M. leprae by binding to DNA. P.o. and accum in fatty tissue w/t1/2 = 90 d.
SE: red discoloration of skin and eosinophilic enteritis.
Antifungal Drugs for subcutaneous and systemic mycoses
amphotericin B
Flucytosine (like 5-FU)
ketoconazole
fluconazole
for superficial mycoses
griseofulvin
Tx systemic mycoses. Used w/ flucytosine to  doses of amphotericin B. Mech: binds
to ergosterol  pores disrupts memb fcn, electrolytes (esp. K) and small molecules to
leak out  cell death. R via  ergosterol content of fungal memb. Spectrum:
Fungicidal/fungistatic. Against candida, Histoplasma capsulatum, Cryptococcus
neoformans, coccidioides immitis, many strains of aspergillus, and Blastomyces
dermatitidis. P’kinetics: i.v.,  Vd except CSF. Intrathecal to tx meningitis if it’s
sensitive to this drug. Biliary exc’n. Plasma prot bound. Long t1/2 = 2 wks. SE: Low
therapeutic index. Fever and chills on 1st i.v. adm. Renal impaiment in 80%+ of pts, rev
but hi dose can cause permanent damage. Hypotension (shock like) along w/
hypokalemia toxicity of digitalis. Need K supplementation. Normochromic,
normocytic anemia by rev suppression of RBC prod, worsened in HIV pts taking
zidovudine. Intrathecal route cause neurological effects.
tx systemic mycoses only in combo w/amphotericin B  synergistic (amphotericin
pokes holes for flucytosine to enter) and prevents R. For subcut chromomycosis, used
alone. Mech: Converted to 5-FdUMP, which inh thymidylate synthetase. Also met to 5FUTP and incorp. into fungal RNA  disruption of protein synth. Spectrum:
fungistatic, tx candidiasis, cryptococcosis, aspergillosis, and chromomycosis. P’kinetics:
p.o,  Vd including CSF. Partial met and renal elim. SE: hematological—reversible
neutropenia, thrombocytopenia, BM, b/c of 5-FU. Hepatic dysfcn. GI.
tx systemic mycoses. Mech: inh fungal P450 inh conversion of lanosterol to
ergosterol. Additive effect w/flucytosine in tx of candida, but antag amphotericin B. No
R reported. Spectrum: fungistatic or fungicidal depending on dose. Most effective
against histoplasmosis in lung, bone, skin and soft tissue even though tissue penetration
limited. Also for nonmeningelal cryptococcosis and blastomycosis, candida, and various
dermatophytic infections (including ones R to griseofulvin). P.o., but absorption need
acidic pH (impaired by food, antacid, cimetidine..) Does not go in CSF. P450 induction.
Biliary exc’n. SE: GI, inh gonadal and adrenal steroid synth  gynecomastia. Allergy,
hepatic dysfcn. Drug interxn: potentiates nephrotoxicity of cyclosporine b/c inh its met.
most recent drug and most useful. Same mech as ketoconazole. P.o or i.v. XBBB of
normal/inflamed meninges. No need for acidic pH for GI absorption. Less P450
induction. 70% drug elim unchanged. Spectrum: Candida, cryptococci, blastomyces, and
histoplasma. Not aspergillus or other filamentous fungi. Drug of choice for crytococcal
meningoencephalitis, disseminated histoplasmosis, and coccidioidomycosis (cond in
immunocomp pts)
disrupt mitotic spindle and inh mitosis. Tx dermatophytic infections b/c accum in
nystatin
Miconazole
clotrimazole
econazole
tolnaftate
infected, newly synth, keratin tissues = hair and nails. LT therapy need until normal
tissue replaces infected tissue. R via lack of E dependent uptake. Spectrum: fungistatic.
Effective against Trichophyton, microsporum, and epidermophyton. Tx severe refractory
tinea infections. P’kinetics: p.o. enhanced if w/ high fat diet  better uptake as micelles.
NOT effective topically. P450 induction and renal elim. SE: safe but can cause allergic
rxn, headache and nausea, hepatotoxicity rare, potentiate effect of alcohol b/c its slight
CNS depr, teratogenic in lab animal, CI in pts w/ acute intermittent prophyria b/c  heme
synthesis along w/  P450.
related to amphotericin B. Restricted to topical tx of candidiasis (oral, vaginal and
Candida esophagitis) b/c systemic tox. Never i.v.. B/c not absorbed p.o, given p.o. for
local oral and intentinal candidiasis.
OTC. Topical, rarely i.v. b/c severe tox. Prop similar to ketoconzaole. Tx Candida and
superficial dermatophyte infections like ringworm
topical against dermatophytes but not against Candida. Mech unknown and no tox.
Antiviral drugs
Tx of Resp viruses
amantadine
Rimantadine
ribavirin
Tx of HSV
acyclovir
valacyclovir
famciclovir
Vidarabine
idoxuridine
prophylactic against influenza A. (ineffective after 48 hrs of exposure) Weak base buffer
in endosome  prevent acidification needed for uncoating of virus. Influenza B lacks the
M2 protein needed for amantadine to bind to. R not common, but via mutations in M2.
P’kinetics: p.o,  Vd including CNS. Not met. Renal elim. SE: CNS: insomnia,
dizziness, headache. Hallucinations and seizures. Antichol  CI in pts w/ glaucoma and
urinary rentention, and in pregnant women.
struct analog. Does NOT XBBB  NO CNS SE.
synthetic guanosine analog. Broad spectrum. Mech: Adenosine Kinase P  furter P
to triP deplete GTP  inh GTP dep capping of mRNA  inh viral prot synth, also inh
virus RNA pol. Rhino and entero have preformed mRNA  R. Spectrum: for infants
and young children w/ severe RSV causin bronchopneumonia. Maybe Hep A and influ A.
Also  mortality and viremia of Lassa fever. Given p.o., i.v., and aerosol. Vd except
CNS. No more met, then renal elim. SE: Bronchospasm in asthmatic pts. In HIV pts,
CNS, GI, dyspnea, extravascular hemolysis. Dose dep macrocytic anemia after 2wks of
therapy. Teratogenic and CI in pregnant women.
all nucleotide analogs, work on acute phase of infection, not latent phase.
guanine analog mono P by viral thymidine kinase. Further P by host kinase. TriP gets
trapped  incorporated into viral DNA  premature DNA chain terminat’n; or binds to
viral DNA pol  inactiv pol; Comp inh DNA pol. Altered thymidine K and DNA pol
confer R. Spectrum: HSV-1+2, and VZV. EBV and CMV R b/c lack thymidine K.
Drug of choice for herpes simplex encephalitis,  survival better than vidarabine. Most
common, tx genital herpes infections. P’kinetics: p.o, i.v., or topical.  Vd, XBBB.
Partial met and partial renal elim unchanged. SE: GI distress and headache from p.o.
Renal dysfcn from i.v. Local irritation from topical.
100% bioavailability  can be p.o., wheraeas acyclovir 30% bioavail, should be i.v..
new acyclovir analog
most effective of the nucleotide analogs and least toxic. Adenosine analog convered to
triP. Selective effect on virus. Mech: Inh virus DNA pol (alter struc confer R), virus
ribonucleotide reductase, and incorporation into viral DNA. Spectrum: HSV 1+2, VZV.
Used for herpes simples keratitis, encephalitis, and VZV in immunocomp pts. P’kinetics:
i.v. over long time and in large vol b/c lo solub. XBBBfor HS encephalitis. Ointment
for herpetic and vaccinial keratitis and HS keratoconjunctivitis. Met in liver and renal
elim of changed/unchanged forms. SE: CNS fxs harmful in pts w/ hepatic or renal
dysfcn.
restricted to topical use b/c systematic toxicity. Thymidine analog. Incorporated into
ganciclovir
AIDS
zidovudine (AZT)
zalcitabine (DDC)
didanosine (DDI)
stavudine (Zerit)
lamivudine
Atovaquone
Protease inh
saquinavir
ritonavir
indinavir
nelfinavir
Miscellaneous
trifluridine
fluorouracil
Foscarnet
viral and mammalian DNA  systemic teratogenic and mutagenicity. SE assoc w/topical
use  conjunctiva contact  irritation, pain, itching, and photophobia.
acyclovir analog for CMV in immunocomp pts. 1’ for CMV retinitis. Mech similar to
ones above.  Vd after i.v. Accum in pts w/ renal failure. Most serious SE = dose dep
neutropenia.
AZT P by mammalian thymidine K, then incororated into viral DNA by RT  chain
term. AZT monoP inh P of dTMP to diP. Also inh host DNA  Pol only @ v. high conc
 lo tox. P.o. and XBBB. Met to glucuronide and t1/2=1hr. SE: BM  anemia and
leukopenia. CNS  headaches, seizures, enhanced by other drugs that are also
glucuronidated, such as probenecid, acetaminophen, lorazepam, cimetidine and
indomethacin.
analogs for pts intol to AZT. Neurological SE.
analogs for pts intol to AZT. Less toxic than AZT to BM but caused fatal pancreatitis.
New AZT analog. t1/2 = 3-6 hrs. Neuro SE
New AZT analog. t1/2 = 3-6 hrs
antiprotozoal for acute oral tx of PCP in pts intol to trimethoprim-sulfamethoxazole.
Mech: ubiquinone like inh ETC  inh synth of nucleic acids and ATP.
used in combo w/ RT inhibitor, otherwise develop R. All met by P450. Don’t give
terfenadine or astemazole.
topical
topical. Esp for warts.
new. Inh DNA pol and RT, and active aginst HSV, CMV, HIV and hepadna virus.
Antiprotozoal Drugs
chemo of amebiasis
metronidazole
Diloxanide furoate
Paromomycin
chloroquine
Emetine
hydroemetine
Chemo of
Leishmaniasis
sodium stibogluconate
tx both acutely ill pt and asymptomatic carriers to prevent relapse or infectious state.
Intestinal amebae feed onnormal flor  tx w/ antibiotics to elim flora. Antibiotics must
be used w/antiprotozoal drugs.
mixed amebicides. Both luminal and systemic. Combo w/ luminal amebicidal such as
diloxanide furoate  cure rate > 90%. Toxic for amebae, anaerobic org including bact,
also anoxic/hypoxic cells. Binds to prot in ETC in protozoa and inh DNA/RNA synth 
cell death. Drug of 1st choice for E. histolytica, Giardia lamblia, Trich vaginalis. Tx
infections by anaerobic G+ and G-, and brain abcesses caused by them. p.o,  Vd
including CSF. P450 met. SE: GI, unpleasant metallic taste. Oral moniliasis or
candidiasis and neurotoxicity (dizziness, vertigo, and paresthesias in PNS. Disulfram rxn.
luminal. Drug of choice for asymptomatic carrier, intestinal amebiasis. Rapid
hydrolysis and inactivation in lumen. SE mild: fart, dryness of mouth, pruritus and
urticaria.
luminal amebiasis/tapeworm, since not absorbed p.o. Aminoglycoside. Direct amebicidal
(cell memb damage and leakage) and by destroying flora. SE: GI distress and diarrhea.
systemic. W/metronidazole and diloxanide furoate to tx and prevent amebic liver abscess.
Also elim trophozoites in liver abscesses in malaria.
systemic. 2nd line drug b/c toxicities. Close monitoring. SE: pain at site of inj, nausea,
cardiotoxicity, neuromusc weakness, dizziness, and rashes.
sandflies transfers promastigote  phag by Mphage changed to nonflagel amstigotes
 kill cell  newly released amastigote phag and cycle cont.
antimony deriv effective only in vivo. Inh parasite glycolysis. I.v. and renal elim unmet.
SE: GI and cardiac arrhythmias.
Chemo of
Trypannosomiasis
melarsoprol
pentamidine
nifurtimox
suramin
Chemo of
toxoplasmosis
Chemo of malaria
primaquine
Chloroquine
quinine
mefloquine
pyrimethamine
chloroguanide
der of mersalyl oxide. For trypanosomes only. Reacts w/ SH on prot in both org and
host. Parasitic enz more sensitive, and mammalian cells less permeable. R via 
permeability. Slow i.v., caution b/c local irritation. XBBB. Drug of choice to tx T.
rhodesiense, which rapidly invades CNS, and in meningoencephalitis caused by T.brucei
gambiense. Rapid oxidation and inactiv  short t1/2. SE: CNS, hypersensitivity,
vomitng, ab pain. CI in pts w/ G6PD def.
Drug of choice in prevention and tx of nematologic stage of T. brucei gambiense.
Mech: E, hi affinity uptake. Bind to parasite’s DNA and  glycolysis. R via no uptake.
Spectrum: Drug of 2nd choice in tx PCP. Trimethoprim-sulfamethoxazole =drugs of 1st
choice for PCP. Tx systemic blastomycosis. P’kinetics: i.m. or aerosol. No i.v. b/c
cause abrupt  BP and tachy. Conc and stored in liver and kidney for long time  tissue
damage. No XBBB. Not met and slow renal elim. SE: serious renal dysfcn but rev upon
w/drawal.
experimental. Tx only T. cruzi. Suppressive rather than curative. Serious SE: CNS,
hypersensitivity, GI.
1’ in tx and esp prophylaxis of African trypanosomiasis. Inh metabolic enz. Drug of
choice for filarial parasite such as Onchocerca volvulus. SE: GI, shock,
unconsciousness, acute urticaria, and neuro.
Drug of choice = pyrimethamine. Combo of sulfadiazine + pyrimethamine also effective.
Other folate synth inh ineffective.
tissue schizonticide. Used in combo w/blood schizonticide. Eradicates 1’
exoerythrocytic forms of P. faciparum and P. vivax and 2’ exoerythrocytic forms of
recurring malarias (radical cures of vivax and ovale). Gametocidal for all 4 plasmodia.
Mech: oxidizing metabolites  schizonticidal, toxicities of hemolysis and metHb.
P’kinetics: p.o, but does NOT conc in tissues. Renal elim of active/inactive metabolites.
SE: hemolytic anemia in pts w/ G6PD def. Ab pain when given w/ chloroquine.
blood schizonticide. Enters RBC and blocks protozoal DNA and RNA synth. Uptake by
binding to ox. heme, formed from Hb in infected RBC  memb damage and lysis of both
parasite and RBC. R via  drug efflux. Spectrum: 1’ drug for tx falciparum. Highly
selective for asexual form of vivax and faciparum. Also tx extraintestinal amebiasis.
P’kinetics: p.o, conc in RBC, liver, spleen, kidney, lung and other tissues, XBBB. P450
met. 4 d of therapy needed for total cure. SE: very little at lo doses. Visual disturbances,
e.g. blurred vision and difficulty in accomodation.
blood schizonticide. For malarial strains R to other drugs. Used in combo
w/pyrimethamine, and sulfonamide. SE: cinchonism = nausea, vomiting, tinnitus, and
vertigo.
blood schizonticide. Suppress and cure mutlidrug-R forms of P. falciparum. Damgae
parasite memb. Extensive met and feces elim. SE: @ hi dose, GI, CNS—dizziness,
disorientation and depr.
blood schizonticide for radical cure and sporonticide in mosquito’s gut. Inh
plasmodial dihydrofolate reductase. Used alone for P. falciparum. In combo w/
sulfonamide, against P. malariae and Toxoplasma gondii.
blood schizonticide and sporonticide. Antifolate. Rapid emergence of R limits use.
Antihelmintic drugs
Tx for nematodes
mebendazole
roundworms w/complete dig tract, including mouth and anus
synthetic benzimidazole, against wide spectrum of nematodes. Drug of choice in
infections by whipworm (tricuris trichura), pinworm (Enterobius vermicularis), and
hookworm (Necator americanus, ancylostoma duodenale). Mech: bind and interfers w/
synth of microtubules   glc uptake. Affected parasite expelled in feces. Poorly
thiabendazole
Pyrantel pamoate
diethylcarbamazine
ivermectin
Tx of trematodes
praziquantel
oxamniquine
metrifonate
Tx of Cestodes
niclosamide
absorbed from GI  local action w/ little SE. @ hi doses, small amt of drug absorbed 
rev alopecia and neutropenia. CI in pregnancy b/c teratogenic.
also synthetic benzimidazole. Against strongyloidiasis cutaneous larva migrans (creeping
eruption) and trichinosis (Trichinella sprialis), and strongyloides stercoralis (threadworm).
More serious SE: readily absorbed from GI  nusea, vomiting, anorexia, and dizziness.
Severe allergic hepatitis when used for > 2 d, as in severe infestation of sm. intestine.
tx roundworm (Ascaris lumbricoides), pinworm, and hookworm. Poorly absorbed
from GI. Depolarization Persistent activation of nicotinic R  paralysis  expulsion
of helminth.
Drug of choice in filariasis (Wuchereria bancrofti, Brugia malayi). Mech:
immobilization of parasitesparalysis. Alter helminthes surface memb  more
susceptible to host immune system. Rapidly absorbed from GI, partially met, and renal
elim. Dying parasites cause pruritus and wheals, systemic cond such as GI, jt pain, fever,
swelling of inguinal lymph nodes and chorioretinitis.
control nematodes in animals by stim GABA R  paralysis. Tx Onchocerca volvulus in
humans. Recently shown that ivermectin better than diethylcarbamazine in W. bancrofti
and B. malayi.
No mouth/dig tract
Drug of choice for all forms of schistosomiasis.  permeability to Ca  easier for Abmediated adherence of leukocytes to kill helminth. Rapidly absorbed after p.o. and distrib
to CSF. Extensive liver met and short t1/2. SE: drowsiness, dizziness, malaise, anorexia
and GI. Most pts no SE.
Largely replaced by praziquantel
drug of choice. Cysticercosis in CNS treated w/prednisone or dexamethasone. Mech:
uncouple ox phos in mito of parasites and host. Absorbed by gut-dwelling cestodes but
not nematodes. Novel ETC in parasite susceptible to niclosamide  paralysis 
expelled with feces. NOTE: must give laxative first to expell dead segment to prevent
release of eggs, which may lead to cysticercosis. SE: minor: ab discomfort, malaise,
fever, some pruritis.