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Drugs of the ANS

Drug type Drug Mechanism Clinical Use Side Effects

Cholinergic Methacholine -Agonist of muscarine CV SPLUDS-BBB

Agonist receptor -Lowers BP & HR -Salivation, Miosis, Lacrimation,
(Muscarinic) -Slows conduction thru AV node Urination, Defacation, Sweating, -
only used in bronchial Bronchoconstriction, Bradychardia
reactivity testing NOTE: Sweating is the only
Sympathetic action here
Carbechol -Direct stimulant of RARE USE THERAPEUTICALLY
muscarine & nicotinic Eye
receptor -Potent & long duration
-NOT degraded by ACh- -Relieve glaucoma
esterase -After cataract surgery
Bethanechol -Muscarinic only GU Generalized ACh-esterase
-Not degraded by ACh- -Stimulate atonic bladder stimulation
esterase (urinate)
-Increase motility
-Esophageal reflux relief
-Post-op ileus tx

Pilocarpine -Stimulates muscarine -DOC for decrease of CNS – disturbances

receptor intraocular pressure in glaucoma Stimulates sweating (10 mg à 3L)
-Crosses the BBB tx
-Xerostomia tx – post radiation
tx etc.
Anticholinesterase Physostigmine -Indirect acting GU/GI Hi dose
(ACh-esterase) (depends upon ACh -Increased motility -CNS – convulsion
Reversible presence) -Miosis (constriction) -Paralysis of skeletal muscle (too
Potentiate Ach -Reversible inhibition of Major use much ACh)
Actions ACh-esterase -Decreases ocular pressure
(therefore, -Acts on all ACh (glaucoma)
counteracts anti- receptors Overdose tx
cholinergics) -central actions -Atropine, phenothiazine, TCA
Neostigmine -Reversibly inhibits GI/GU -Generalized ACh stimulation
ACh-esterase -Stimulates motility
-Doesn’t cross BBB -Antidote for tubocurarine
-NO Pupil constriction -Tx for myasthenia gravis (b/c
-orally active no CNS effects & long life)
Edrophonium -Similar to neostigmine - Used in dx of myasthenia -Generalized ACh stimulation
Short half life gravis Cholinergic crisis – antidote is
-tests: better =MG Atropine
worse= cholinergic crisis
Irreversible Covalently binds to ACh- -Glaucoma only in very very CNS
Organophosphates esterase dilute solutions -Confusion, ataxia, slurred speech,
DFP/Echothiphaat -Nerve gas & -Tounge Fasiculations loss of reflexes, convulsions, coma,
e insecticides respiratory paralysis, death
Slow Reversible Antidote – Pralidoxime
Malathion, /ATROPINE
parathion, soman,
tabun, sarin
ACh-esterase re- Pralidoxime Binds to ACh-esterasee Overdose of organophosphates -Only effective in short time period
activator (2-PAM) inhibitor to pull it from -Blocks SLUD (salivation, after AchE conversion. New nerve
enzyme lacrimation, rination, Defecation) gases have very short window of

Cholinergic Atropine Competitive antagonist Eye Dry – lo sweat/salivation
Antagonist to muscarinic receptor -Cycloplegic & myadriatic (near -Dilated w/ loss of accommodation
accommodation/dilation) -Flushing of skin
GI/GU -Hot (no sweat i.e. no
-Antispasmodic thermoregulation)
-Antidote for organophosphates -Delusions & toxic psychosis
-Decrease acid productin (peptic
ulcer tx)
-Antisecretory for surgery
Anesthetic – decreases
-Tx of parkinsons

Scopolamine -Competitive blocker of DOC-Motion Sickness Atropine-like

muscarin receptors (prophylactic)
-Greater action on CNS
w/ longer duration
Tropicamide Competitive antagonist Eye exam Atropine-like
to muscarinic receptor -Cycloplegic& myadriatic
Ipatropium Competitive antagonist Anti-asthmatic, COPD (topical Atropine-like
to muscarinic receptor inhaler)
Pirenzepine Ulcer tx
Benztropine -penetrates CNS Parkinson’s Disease (central
Cholinergic Trimethaphan -Short-acting blocker -Reduces HTN & prevents -Blocks all autonomic responses
antagonist reflex tachycardia -Orthostatic hypotension
(Nicotinic) -Good for pt. w/ aortic -Tachycardia (blocks
--Ganglionic dissecting anuerysim. parasympathetic reflex)
blockers-- -Decreased GI/GU motility, à
urinary retention, constipation
Hexamethonium Experimental only

NM Blockers Tubocurarine Competitive nicotinic -Flaccid paralysis – 30-60 min

Succinyl choline Nicotinic receptor -Initial fasciculations
agonist -Short acting: deactivated by
-Depolarizing butyryl ChE in serum
Adrenergic Epinephrine -Interacts w/ both DOC – CNS – anxiety, fear, tension, h/a,
Agonist alpha & Beta receptors bronchospasm/anaphylaxis tremor
a>b2>b1 Eye Hemorrhage – cerebral via hi BP
-Glaucoma – decrease pressure Cardiac arrhythmia – esp. in digitalis
IE: Non-Specific via vasoconstriction of ciliary pt.
-alpha: vasoconstrict blood vessels Pulmonary edema
-beta1:^HR and -Increase duration of
contractility anesthetics via vasoconstriction
-beta2: bronchodilation -Low dose, MAP stays the same
(increase sys, decrease dias) hi
dose MAP increase
Norepinephrine a>b1>b2 Shock –powerful vasoconstrictor
-Less pulmonary action -Not good enough for
than w/ epi bronchodilation

Isoproterenol b2>b1>>>a Bronchodilator -Similar to epi but more potent
-i.e. non selective beta- Stimulate heart -Discontinued from due to deaths
agonist Decreases peripheral resistance from CV involvement
(can distinguish b/w b/c no association w/ alpha
beta and alpha rectp.) receptor
Dopamine Precursor ofr NE Shock – increases BP, enhances Hi dose – arrhythmia
DA>b1>a1 perfusion to renal (SPARING), Similar to epi
splanchnic & coronary arteries DA converted to HVA which can
CHF – contribute to increasing cause
CO Nausea/hypertension/arrhythmia
b1 agonist Dobutamine B1 selective agonist CV Use w/ caution w/ pt. in A-fib
-CHF tx – increase CO w/ little DOBUTAMINE –
-Shock/resucitation – increases DOPAMINE -- HYPOTENSIVE
force more than rate
B2 selective Metaproterenol B2 agonist Lungs -Adverse affects of B2’s
agonists -Little effect on heart -Bronchodilator – asthma --Skeletal muscle tremor,
-Resistant to COMT -Relaxes uterus to prevent restlessness, tachycardia,
Note: Not methylation/degradation childbirth arrhythmia, pulmonary edema in
Specific pregnancy, increased death rate in
Terbutaline B2 agonist SAME
/Albuterol -More selective than
Ritodrine Same -Primarily against premature CAUTION:
labor -Hyperglycemia in mother &
reactive hypoglycemia in newborn
-Contraindicated in IDDM pt.s
-Risky – CV effects
b1/b2 nonselective Propanolol b1&b2 blocker MAJOR USE: -Contraindicated in acute CHF b/c
antagonists NOTE: don’t give to -Essential Hypertension, cannot give drug to increase CO
pt. w/: heart failure, arrhythmia, --Rebound tachycardia if suddenly
asthma, diabetes -Migraines – blocks catechlamine removed
induced vasodilation in brain -ASTHMA IS ABSOLUTE
-Hypethyroidism – blocks -Exercise intolerance – can’t
periphera conversin of T4 to T3, increase CO
decrese sympathetic stimulation -Decreased HR
from hyperthyroidism -Exacerbate CHF
-Angina pectoris – reduction of -Conduction slowing
O2 requirement of heart -Incease TAGS (LDL)
-MI-reinfarct protection -Sexual dysfxn
-Glaucoma -Delays response to hypoglycemics
Naldol Longer acting pure
-No CNS involvement
Timolol Glaucoma – reduced ciliary -Watch for systemic effects
epithelial humour production
Labetalol -Also A1 antagonist Hypertension – peripheral Orthostatic hypotension
vasodilator. Decrease BP w/o Dizziness
altering TAG or glucose
-Antihypertensive w/o reflex
b1 selective Metaprolol/ Anti hypertension/ sympathetic Similar to propanolol
antagonist atenolol cardiac overstimulation

Esmolol -Very short t1/2 -Use in ill pt.s where risk of
hypotension or heart failure is
-If they start to die, fine…. just
stop giving the med

A1 selective Phenylephrine/ A1>A2 Tx of mydriasis, hypotension
agonists Methoxamine/ -Slow metabolism w/ --- vasoconstriciton
metaraminol little CNS penetratin -Nasal decongestant – prolonged
-Eye drops – decrease redness
via vasoconstriction
-Termination of paroxysmal
atrial tachycardia (via vagal
A1 antagonists Phenoxybenzamin Nonselective Decrease BP Only mechanism to overcome is by
e -Irreversible covalent -Tx for pheochromocytoma- making new adreno-recptors, which
linkw/ A1 post synaptic induced hypertension. Causes takes approx 24 hrs.
& A2 presynaptic reflexive incrase in CO from -Postural hypotension
receptors blocked A2 & B1 system -Nasal stuffiness
overrides -Nausea, vomiting
-For dx of pheochromocytoma -Ejaculation problems (shooting
-Frostbite blanks)
-Clonidine w/drawal
-Raynaud’s phenomena
Phentolamine Nonselective Same but reversible
-Blocks A1 & A2
Prazosin Highly A1 selective Decreases BP w/ no reflex Orthostatic hypotension (u’ll get
tachycardia suPRAZed when u stand up)
Antihypertensive -Vertigo
-Nasal congestion
Terazosin A1 selective Tx of BPH-associated urinary
-Relaxes SM of prostate

A2 selective Clonidine -Decreases central NE Hypertension Sedation

agonists -Minimize sx from w/d from -Orthostatic hypotension
opiates, cigarettes & BDZ’s w/d sx include hi BP, h/a, tremors,
-Rx’s heroin’s anti-adrenergic sweating, tachycardia
-Decreases sympathetic activity
MISCELLANEOUS Amphetamine/ -A & B receptors
ritaline -Promote NE release
-CNS target
Ephedrine -Same as above -Included in many cold medicines
-CNS is side effect
Reserpine -Prevents cytosolic -Reduces reuptake of NE -Side effects limited by using low
reuptake of NE into -Effective, cheap dose (Depression)
vesicles antihypertensive
Cocaine Block reuptake of NE -Used socially
-Amplifies any
peripheral or central

Drug Epinephrine Norepinephrine Isoproterenol
A & B Agonist B selective
Pulse rate Increase Decrease (reflex Increase
MAP Same Increase Decrease
(Increase sys, (lg. Decrease sys,
decre mild
ase increase
dias) sys)
Peripheral Decrease Increased Decrease
resis (Vasoconstriction) (Significant)


Drug Mechanism Clinical Use Side Effects

Histamine Diphenhydramine H1 & H2 antagonists -Allergic rhinitis/urticaria Sedation – antagonize

antagonists Chlorpheniramine -Also antagonize ACh, -Motion sickness (scopolamine muscarinic/serotonin
H1 & H2 NE, Serotonin in CNS is better) Dry mouth
-Diphyd – also good -Sedation (side effect) Potentiates effects of other CNS
local anesthetic that -Sleep induction depressants (alcohol etc)
reverses effect of **Not used in bronchospasm** Loss of appetite, nausea, distress,
phenothiazines constipation or diarrhea
H1 selective Fexofenadine Selective H1 Allergic rhinitis (daytime PVC’s – tachycardia
Antagonist Larotidine -No sedation (doesn’t benefits) Prolonged QT interval
cross BBB) Liver dysfxn
H2 antagonist Cimetidine -Selective H2 blocker Gastric ulcer Mainly Cimetidine
(tagamet) in stomach & blood Zollinger-ellison syndrome -Inhibits P450
Ranitidine vessels Gastro-esophageal reflux -h/a, dizzy, diarrhea,
(xantac) -Ranitidine, (GERD) -Lowers sperm count
Famotidine famotidine are more Hiatal hernia Anti-androgenic
(pepsid) potenet than -Gynecomastia, lo sperm count
cimetidine & don’t -Galactorrhea
inhibit the P450 syst,
longer acting & less
side effects
Serotonin Methysergide -Congener of LSD -Migraine – prophylactically -Toxic effects limit use
antagonist which antagonizes 5- Carcinoid sndrome -Leads to fatal pulmonary/cardiac
HT receptor fibrosis if used chronically
HT1 blocker Cyproheptidine Blocks 5-HT2 to Post gastric dumping syndrome Sedating due to H1 Block
block SM Vasospastic disease- trials
contractions May be used as antihistamine
Also blocks H1
HT2 blocker Ketanserin -Highly selective Hypertension – trials
-Also blocks a1 Vasospastic disease – trials
HT3 blocker Ondansetron HT3 blocker Cancer chemotherapy (anti-
emetic) – prevents N/V
Busipirone -HT1 partial agonist, Anxiolytic Non-addicting
DA2, HT2 blocker No cross tolerance w/ alcohol
Serotonin Cisapride HT4 agonist in GI GERD
Sumatriptan HT1 agonist Migraine acute tx Cost
-More effective than ergots
(ergonovine, methylergonivine,
ergotamine –used in postpartum
-Tingling/flushing @ injection site
-Chest tightness, angina in CAD
SSRI Fluoxetime Inhibits receptor Depression Weight loss
(Selective (Prozac) mediated uptake of Insomnia
serotonin 5HT to increase Flushing, sweating
reuptake serotonin levels GI disturbances

Adenosine Adenosine Inhibits all excitable Paroxysmal Supraventricular -Receptors through out body
cells tachycardia -Anginal pain – vasodilation
-Esp. AV node -DOC after failure of valsalva type -Asystole (watch dose)
-Involved in maneuvers --Luckily short acting drug
autoregulation -Diagnostic & curative -Contraindicated in pt. on dipyridamol –
Adenosine stress test – for those potentiates affects (theophylline is
unable to jump on the stairmaster antidote)

Adenosine Methylxanthines -Intereferes w/ Ca++ CNS Stimulant Anxiety, agitation

Antagonists (Theophylline, binding by SR Increased HR & CO Insomnia
caffeine, -Inhibits Asthma – theophylline Arrhythmias
theobromine) phosphodiesterase to
prevent increase of
Adenosine Dipyramidole -Blocks adensine -Tx angina pectoris Do not give adenosine while on this drug b/c
agonists reuptake -Inhibit emboli from prosthetic valve pt. may arrest
-i.e. increases levels
(increases cAMP)
Ergotamine/ Agonist @ alpha Termination of migraine headaches Avoid over use (rebound migraine)
dihydroergotamin adrenergic &
e serotonin receptors
Prostaglandins Misoprostol PGE1 analog – GI protection from NSAID-induce
increased mucosal ulcers
resistance to injury -Ductus arteriosus opener
-Inhibits secretion of -Used w/ methotrexate in terminating
HCl in stomach & pregnancy in 1st trimester
inhibit gastric acid &
gastrin secretion
Leukotrienes Zileuton Inhibitrs 5- Asthmas-tx
lipoxygenase -Cold, NSAID, exercise induced
Zafirlukast Blocks receptor for Same

Drug Mechanism NSAIDS Clincal Use Side Effects

NSAIDs Aspirin Irreversible Analgesia – not visceral pain GI bleed

acetylation of cyclo- Fever – no affect if no fever present -Uric acid excretion – competes w/
oxygenase (offsets PGE2) excretion/reabsortptionHi risk of gout
-prevents formation Inflammation Reyes syndrome
of PGE, TXA2, Anti-platelet coagulation Liver toxicity
Prostacyclin Increased survival post-MI Hypersensitivity
-deacetylation à Edema, Hi K+
salicylate which is anti-
Salicylism – tinnitus, dizziness, h/a,
-blocks PG
Overdose à hypercapnea (increased sens.
To CO2 receptors)à alkalosis, deranged
metabolism à acidosis(CNS & resp.
depression), hyperthermia, N/V, sweating,
hypovolemia, petechia
Overdose tx --- fluid, glucose, HCO3-, K+,
cooling, diuresis, lavage, charcoal
Ibuprofen -same potency as Inflammatory diseases GI disturbances
aspirin Dysmenorrhea Tinnitus
-hi analgesia & Rashes
antipyretic properties H/a
-reversible inhibition Interstitial nephritis
of cyclo-oxygenase
Naproxen Longer-acting
derivative of ibuprofen
Indomethacin More potent cyclo-
Closes ductus arteriosis Aplastic anemia
oxygenase inhibitor
-no increased bleeding Only effective in Hodgkin’s fever Acute renal failure
time N/V h/a
Ankylosing spondylitis
Acute pancreatitis
Gouty arthritis
Pre-term uterine-contraction reduction
Phenylbutazine No longer used Bad side effects (BMS)

Tolmetin/piroxica Long t ½ More potent than aspirin <than aspirin

Meloxicam/ Selective cyclo- Peripheral jt.s in diseases like RA & Little GI disturbances
peroxicam oxygenase 2 inhibitor osteoarthritis Renal toxicity
Sulindac Pro-drug (hepatic Gouty arthritis Agranulocytosis
activation) Pre-term labor
- Decreases adenomas w/ FAP
Ankylosing spondylitis
Keterolac Injectible form Same as other NSAIDS
Post-op pain –visceral
Like opiates w/o CNS
side effets Allergic conjunctivitis
Non- Accetominophen Non-anti- Analgesia Hepatotoxic @ hi concentration
NSAID inflammatory Fever Acetylcystein is antidote (sometimes
Inhibits Good for pt. on probenecid & uricosuric cimetidine)
cyclooxygenase only in for gout b/c no X-tolerence

GI Drugs

Drug Mechanism Clinical Use Side Effects

Peptic Ulcer Cimetidine -Blocks gastric mucosal -Zollinger-ellison syndrome Primarily Cimetidine
H2 agonists (Tagamet) histamine receptor to (relapse of ulcer after short- -Many drug interactions
Ranitidine decrease acid output term tx or abrupt cessation) -Decrease hepatic blood flow
(Zantac) -Acts to increase gastric pH -GERD -Inhibit P450
Famotidine & decrease pepsin formation -Peptic ulcers-hiatal hernia -Anti-androgenic effects
(Pepsid) -Tylenol O.D. (Cimetidine) (gynecomastia)
Nizatidine -CNS (elderly) – confusion &
(Axid) drowsiness
-Skin rash
Muscarinic Prienzepine -Atropine-like compound have -Adjuncts to histamine receptor -Same as atropine
Antagonists only small ability to decrease blocker tx
gastric acid -Not currently used
-Doses cause more side
effects than benefits
Omeprazole -PPI DOC – Z-E Syndrome H/a, dizzy, nausea
-Converted to active form Histamine resistant ulcers -Abd. Pain
(sulphamide) Reflux esophagitis -Long term use may be
-Covalently binds H/K ATPase H. Pylori infection carcinogenic due to hi gastrin
on mucosal side of parietal levels
cell -Hyperplasia of oxyntic mucosal
Misoprostol PGE1 receptor agonist -Prevent NSAID-induced ulcer -Diarrhea
-Gi protein decreases cAMP & -Gastric ulcer -Abdominal pain
inhibit basal & stimulated acid -Duodenal ulcer -Contraindicated in pregnancy
secretion -Abortiion w/ (MTX)
-Enhances mucosal barrier by
increasing mucus & NaHCO3
Sucralfate -Cytoprotective -GI ulcers & erosions No major side effects
-Combines w/ protein -Stimulate PGE production -Alterss bioavailability of other
exudates @ base of the ulcer -Promotes healing (increase drugs
& forms a resistant barrier cell#) -“Large Pill” compliance
(won’t adhere to normal -Constipation
tissue) -Antacids decrease its efficacy
-Coats for >5 hr.s
-Doesn’t effect acid
secretion & absorbs pepsin
Antacids Na-bicarbonate Immediate onset Belching
-Short duration Systemic alkalosis
-May increase gastric pH to Sodium retention
alkaline level which increases
HCl secretion
Ca++ Carbonate Rapid onset Esophagitis Systemic alkalosis
Duodenal ulcer Phosphate imbalance
Gastric rebound
Mg++ Salts Mg(OH)2 – milk of magnesia Osmotic diarrhea
Relativelyinsoluble à slows Hypermagnesemia
removal from stomach Belching
Al3+ Hydroxide Least potent Used in combo w/ other antacids Constipation b/c AlCl3
Reacts w/ HCl to produce Binds phosphates
Anti-emetics Phenothiazines Blocks DA receptors in Cisplatin induced N/V Sedation
Prochlorperazine chemoreceptor zone Poisons & visceral afferent pain Parkinson-like

Diphenhydramine Blocks H1 & H2 Motion sickness Sedation
Allergic rhinits/urticaria Don’t give w/ other CNS
Sedation depressants
Dimenhydrinate Antihistamine agent that also Motion sickness (inner ear) Sedation
Cyclizine blocks ACh receptors Vestibular inflammation
Canabanoids U/k mechanism N/v associated w/ cancer, Hi abuse potential
Nabilone Dronabinol is major chemotherapy Drowsiness
Dronabinol (THC) component of Vomiting caused by higher Ataxia
weed/hash/gangi/dope/hemp/ centers 0 emotions, signts Inability to concentrate
u get the picture smells Disorientation
-Works in higher (yeeaaah!) Glaucoma Anxiety
centers in brain Psychosis
Laughter (that horrible stuff….)
Metoclopramide DA antagonist w/in CNS & N/v associated w/ ca Fatigue
(Reglan) ACh agonist w/in GI chemotherapy Insomnia
-Simultaneouslyy inhibits -Reflux esophagitis Parkinson-like
vomiting centrally uremia Acute dystonic rxn
-Enhances UGI motility Extrapyaramidol sx
Ondansetron Serotonin antagonist Ca chemotherapy esp. w/ H/a
-Causes colonic motility cisplatin Diarrhea
-Radiation-inducd vomiting
-Post-op N/V
Laxatives Bran Increases mass Laxatives in general: Virtually safe & effective
Softening (1-3 Methylcellulose -In turn stimulates peristalsis -Constipation -If not taken w/ H2O, then may
days) Psyllium increase water content of -Pre-op or pre-radiological exam cause obstruction/impaction
stool -Maintain insulin control contraindicated:
-Increases motility & -Decrease cholesterol -Bowel obstruction
decreases absorption of NaCl decrease colon ca risk undiagnosed abd. Pain
& H2O
Docusate Stool softener May increase intestinal
-Detergent absorption
-Disperse wetting agents that Hepatotoxicity
permit H2O & lipids to enter
the mass & soften it
Mineral oil Penetrate & soften stool Interferes w/ absorption of
Indigestible essential fat soluble substances
Lipid pneumonitis
Lactulose Osmotic laxative that is Systemic toxicity from
noabsorbable which increases electrolyte imbalance
intraluminal osmotic pressure Dehydration
& increase fluid content of Flatulence
Soft/semifluid Diphenylmethans Acts as irritant to colon Limit use for <10 consecutive Fluid/electrolyte deficit
stool (6-8hr.s) Phenolphthalein -Stimulates auerbach’s plexus days Allergic rxn
(exlax) to promote intestinal motility Turns urine/feces pink
Atraquinones Similar to diphenylmethanes May turn urine red
Casarca sagrada
Watery Saline Osmotic or saline laxative Systemic toxicity due to
evacuation that is nonabsorbable which electrolyte imbalance
(1-3 hr.s) Sodium increases intraluminal osmotic Dehydration
phosphate pressure & hi fluid content of
Magnesiu stool


Castor oil Irritant to small intestine Too strong for common Fluid/electrolyte deficits
constipation Decrease absorption of
Uterine contractions
Diarrhea Morphine-like Synthetic opioids that General diarrhea Habit forming
decrease peristaltic bowel AIDS associated diarrhea Not too addicting b/c they are
Diphenoxylate motility & counteract relatively insoluble
Loperamide excessive secretion Promotes ulcer formation
(Imodium) Little CNS action
Often combined w/ atropine
to decrease addiction
Atropine Block ACh receptors to Diarrhea Only produce the atropine-like
Dicyclomine decrease parasympathetic side effects @ hi doses
tone & motility of GI tract
-Antispasmodic action
Bismuth Anti-bacterial action h. pylori diarrhea
Anti-secretory action


Class Drug Mechanisms Side Effects

Clincal Use

DIURETICS Acetazolamide -Related to Glaucoma – dorzolamide -Hyperchloremic

Carbonic Dichlorphenamide dichlorphenamide, topical, acetazolamide in Metabolic Acidosis

anhydrase Dorzolamide Dorzolamide emergency -Renal stones –
inhibitor (Topical for eye) -Urinary alkalinisation enhanced phosphaturia,
-30 min max effect excretion of weak acids calciuria, decreased
-Indirectly block HCO3- (ASA OD) solubility
reabs -Decrease CSF production -K+ loss
-Enhanced K+ secretion -Metabolic alkalosis – -CNS toxicity – hi dose
downstream secondline
-Enhanced NaCl -Acute mountain sickness – CI – cirrhosis à
resorption cerebral edema, resp. hepatic encephalopathy
ACIDazolamide = alkalosis) (NH4+)

Osmotic diuretic Mannitol -Excreted in glomerular -Diuresis -EC volume expansion

filtrate w/in 30 min -Maintain tubular flow/flush (à CHF, Pulmonary
--Retains H2O w/in debris edema)
tubule -Reduce -h/a, N/V
intracranial/intraocular -Dehydration,
pressure hypernatremia

Loop diuretic “high Furosemide -Duration 2-3 hours Edema – pulmonary, CHF Ototoxic – esp. w/
ceiling” Bumetanide -Glomerular filtrate, Acute hypercalcemia, aminoglycoside
Torsemide secretion hyperkalemia Hypokalemic metabolic
Ethacrynic acid -Na/K/Cl transport in Anion overdose – Br-, Fl- etc alkalosis
thick ascending limb Forced diuresis Dehydration
-Direct effects on HTN, CHF – 2nd line tx Allergy
blood flow (renal/ (thiazides #1) Nephritis
pulmonary) Gout
Secretes: Na+, K+, Ca+ OH DANG
+, increased urine

Thiazide Hydrochlorothiazid -Excreted by organic HTN Hypokalemic metabolic

e acid secretory system CHF alkalosis
-Inhibit NaCl symporter Nephrolithiasis – idiopathic HyperGlycemia
in DCT hypercalciuria HyperLipidemia
-ENHANCES calcium Nephrogenic diabetes HyperUricemia
resorption (unlike loops) insipidus HyperCalcemia
Secretes: Na+, K+,
increased urine volume Hyper-GLUC
Retains: Ca++ Hypernatriuria
K+ sparing Triamterene Triamterene – hepatic The K+ STAys Hyperkalemia –
Amiloride met, renal excretion aggravated by B-
Spironolactone Amiloride - renal blockers, ACE-Inh,
excretion -Hyperchloremic
Spironolactone – metabolic acidosis
prodrug of canreonate -Spironolactone –
Mild increase in NaCl Triamterene – acute
excretion in late DCT, renal failure
Collecting duct (+indomethacin), kidney

Uterine Drugs

Class Drug Mechanisms Side Effects

Clincal Use

UTERINE Mifeprestone -PGE-1 analog -Induction of labor upto 7wk.s Uterine bleeding, malaise, rash
DRUG (RU 486) -The morning after (72 hr)
CI: ectopic, COPD, renal/hepatic,
adrenal failure, steroid therapy
PGE2/PGF2a Cause uterine contractions Induce abortion/labor -GI-nausea, vomiting, diarrhea
Topical – ripen cervix -Hypotension-PGE2

CI: asthma, COPD, CAVD

Oxytocin -Milk ejection -Lactation – nasal spray Rare
-Contraction in gravid uterus – -Induce/maintain labor
efficacy increases near term Antidote: fenoterol CI:
-Weak antidiuretic -Control hemorrhage -Fetal distress
(contraction) -Premature
-Test fetoplacental -Cephalopelvic misproportion
circulatory reserve -
Engonovine -a-adrenergic, dopaminergic, DOC: induce p.p. contraction N/ abd pain
serotoninergic (hemorrhage control) H/a
-Lo dose – contract gravid uterus -Prophylaxis Dizziness
(promote labor/stop hemorrhage) -Uterine atony (prolonged Tinnitus
labor/big uterus) Hypertension
Ergotism – necrosis of extremities
Tocolytics (inhibit Ritodrine B2 agonist-high cAMP to relax -Prevention of premature -Maternal tachycardia
uterine smooth muscle of the uterus labor -h/a, vertigo
contraction) -3-6 hr. onset -Relaxes SM in uterus/resp. -Constipation
tract -Fetal tachycardia
Tocolytic indication: uterine -Hypoglycemia in fetus
bleeding, cramping (<20wk.), CI:
premature labor w/ dilation (36 wk.) -
Mg++ sulfate -Prolonged distribution in deep -Tx pre-eclampsia seizure -Bradycardia, delayed AV
compartments -Hypomagnesemia – prevent conduction
-Similar efficacy to B- fetal hypotrophy -Hypotension
sympathomimetics -Adjunct tx of MI -Must monitor, BP, fetal HR,
-Mg++ antagonizes Ca++ -Osmotic laxative reflexes
Ca++ gluconate - antidote
Toxicity: ECG changes à
resp. depression à loss of CI:
corneal reflex -Renal failure, myasthenia, AV
block, before delivery

Antihypertensive Drugs

Class Drug Mechanism Clinical Use Adverse Effects

Diuretics Thiazides See diuretic section -1st line against hypertension -Hyper-GLUC
-CHF –shows the greatest -Hypokalemia – add K+ sparing if this
effect to dec. ventricular is a problem
hypertrophy, morbidity, and
Loop Diuretics & See diuretic section -K+- sparing is 2nd line
K Sparing
NE release Agent Reserpine -Deplete biogenic amines (NE) from Denervation of sympathetics
neuronal storage vesicles (inhibit -60-80% à nasal congestion
reuptake) -Hypersecretion
-Peripheral & CNS -Bronchoconstriction
-Mental depression
Alpha-1 blocker Prazosin -Competitively bocks a1 receptors -Mild HTN -1st-dose Phenomenon:
t ½ 3-4hr. w/out a reflex tachycardia -Low TPR -Weakness and syncope w/in 1hr.
Terazosin -No effect on A2 -Low BP by relaxing arterial after 1st dose. You’ll be suPRAZEd
t ½ 12hr and venous smooth muscle when you stand up.
Doxazosin -Decrease LDL, increase HDL -HTN/BPH use Terazosin -Postural hypotension
t ½ 22hr -h/a, dizziness
Alpha-2 agonist Clonidine -A2 agonist -2nd line tx for HTN -Dry mouth
-Central effects -Other, w/d sx in -Sedation
-Decreases CO, reduce peripheral alcohol/heroin etc. -Orthostatic Hypotension
resistance w/ maintanence of renal -Alcoholic delirium -w/drawal symptoms: Rebound
blood flow -Postmenopausal syndrome (High BP, headache, tremor,
-Therapy-resistant diarrhea sweathing, tachycardia)
- Bradycardia
B-blockers Propanolol -Do not use in asthma, COPD, CI: pregnancy, IDDM,
Atenolol -increase LDL TAGs, decrease HDL CHF, SA or AV node abn (Blocks sympathetic response to
Metoprolol hypoglycemia therefore pt could
Pindolol drop dead due to hypoglycemia with
Labetol no symptoms)

ANGINA Propranolol -Decrease severity/freq of -Cardioprotective post-MI Contraindications
B-blockers Atenolol exertional angina (keep on for 2-3 yr.s) -Astham/COPD
Metoprolol -Ineffective in unstable -May worsen vasospastic -CHF
-(-) Inotropic effect angina -IDDM-see above
-(-) Chronotropic effect Angina associated w/: -Fatigue
-Decreased sys BP w/ exercise Exertional -Can mask hyperthyroidism (inhibits
NET EFFECT: decrease heart O2 Ventricular arrhythmia peripheral conversion of T3 to T4)
demand <40

Ca++ blockers Verapamil Binds serum proteins Angina associated w/: Dihydropyradines
Diltiazem -Hepatic metabolism, renal secretion Vasospastic -Dizzy, h/a, flush, digital dyasthesia,
Nifedipine -Blocks L-type Ca++ receptors – COPD/asthma peripheral edema, constipation,
(dihydropyridine) cardiopressant & vasodilation >65 reflex tachy
-Decrease afterload
-Increased risk of MI in HTN Verapamil, diltiazem – bradycardia,
patient slow SA & AV
Nitrates Nitrates -Relax all SM -HTN Vasodilation: h/a, flush
(Nitroglycerine) -Mostly venous relaxation, some -Acute angina Hypotension: reflex tachy
(Isosorbide arteriolar -Prolonged preventive therapy Dizziness, weakness, cerebral
dinitrate) -Decreased myocardial demand -Spasmolytic in colic pain ischemia
(Isosorbide -Buccal, IV, transdermal, sublingual Tolerance: must give time off b/c
mononitrate) -Decrease preload uses up sulfhydryl system

CHF Medication
CHF Captopril -Renal elmination -1st line drug—Hypertension -Hypotension
ACE-inhibitors -Angiotensin II Antagonist -CHF – decrease sudden death, -Cough/bronchospasm (bradykinin)
-Decreased vasoconstriction, NE, progression, morbidity, -Angioneurotic edema
aldosterone -MI – if started in preinfarct -Hyperkalemia
Bradykinin – vasodilation period -Proteinuria
-No: -Progressive renal disease -Dysgeusia (taste)
-Reflex tachy -Hypercalcemia
-Change in CO -Less efficacious in Black CI – renal artery stenosis, renal
- Na/H2O retention Patients. failure, pregnancy (physical
-Decreased sympathetic tone deformity), hx of angioedema
Vasodilates venous blood vessels to -1st DOC-first line of choice in Toxicity – hypotension w/o
decreased pre-load and aterioles to the Rx of CHF w/ diuretics tachycardia
lower TPR. Decreased Na/fluid Interactions: NSAID (bradykinin
retention pthway), K+ spare/waste diuretic,
increased digoxin, lithium levels
Enalapril/ -Enalapril is prodrug (hepatic -More potent than captopril,
enalaprilat conversion) slower onset, longer action
Fosinopril -Enalaprilat – IV for HPT emergency
Moexipril -Fosinopril, moexipril – only hepatic
CHF Digitalis -(+) Inotropic effect – increased Ca++ -CHF – NYHA III, IV -Arrhythmia, bradyarrhythmiaPVC,
(Digoxin) load via inhibition of Na/K ATPase -A-fib, flutter V-fib, etc. parox/nonparoxysmal A-
-(-) Chronotrophic) via vagal input tach
-Decrease AV conduction (prolong Non-indicated -GI-anorexia, vomiting, diarrhea
ERP) -Myocarditis, cor pulmonale -Neurologic-“digitalis delirium”
-Increased automaticit & excitability -Uncontrolled HTN (headache, fatigue, neuralgia, and
atria, purkinje, ventricles -Bradyarrhythmias mental symp’s)
-Visual disturbances - color
ECG -Gynecomastia – rare
Atria- P changes Tx of digoxin overdose:
AV – PR prolonged -Decrease or w/d drug Precipitating factors for toxicity
Ventricles – short QT, depressed ST, -Monitor dig & K+ levels, ECG -Hypokalemia or hyperkalemia
T -Correct electrolyte -Hypo Mg++, or hyper Ca++
-V-tach – lidocaine, Mg++, K+ (aggravates effects of Dig)
-Decreases morbidity but no effect (take to normal hi), -Resp. disease – increase digoxin
on mortality Severe response
-Temporary pacemaker ->65, skinny, fever
-Digitalis Ab -Acid base imbalance
-Etc, etc, etc
Amrinone Phosphodiesterase inhibitors. -Like coffee it relaxes vascular Milrinone has actually shown to have
Milrinone Increased cAMP which increases (Ca) and bronchial smooth muscle an increase in mortality
I to higher contractility
BETA-AGONISTS Dopamine Increased cAMP, which activates -Acute CHF episode See autonomics
Dobutamine proten kinase to phosphorylate Ca- -Shock -Use with caution in atrial fib.
channels to increased (Ca) I, which -BP up with increased
increases contractility. Also has perfusion to Kidneys,
some vasodilating effects

SELECTIVE Losartan Like ACE-I: decrease -Hypertension NO COUGH b/c there is no

ANGIOTENSIN vasoconstriction, NE release, increased levels of bradykinin
II aldosterone secretion -It may be fetotoxi
Unlike ACE-I: no affect on
degradation of bradykinin

Antiarrhythmic Drugs
Class Drug Mechanism Indications Adverse Effects

Ia Quinidine -Binds to activated Na- Supraventricular Toxicity

channels to prevent Na arrhythmia -Cinchonism (ringing in ears,
influx -DOC-for Chronic headache, altered color
-Block K+ channel (prolong Ventricular Tachycardia perception)
AP & ERP) -Conversion of atrial -Nausea, vomiting, diarrhea,
-Antimuscarin – paradoxical flutter/fib -Arrhythmia (torsade d’pointes)
increase in AV conduction -Shouldn’t be used w/o -High (digitalis)
-alpha blocker (hi digitalization 1st -Decreased contractility
concentration) -Antimalarial

-Depress automaticity ***Toxicity, wide QRS**

(ectopic pacemakers) ECG Changes
-Depress conduction & -wide QRS
excitability (esp. -long QT & changed T
depolarized tissue) -Prolong PR interval
Ia Procainamide Similar to Quinidine. Procainamide – 2nd line Procainamide
Dysopyramine -Acetylated à (NAPA) AMI-associated vent. - SLE-like Syndrome,
(blocks K+ channels)— Arrhythmias (lidocaine – - Agranulocytosis,
control plasma levels of 1st) -Antimuscarinic: aggravate
both (procainamide) glaucoma, urinary retention
-Prolongs the refractory -Mental confusion/ psychosis
-Block active Na+ channel Disopyramide
-Block K+ (esp. NAPA) – Negative inotropy,
-Antimuscarinic – Cardiac failure w/o
-alpha sympholytic existing myocardial
– Atropine-like systemic
Ib Lidocaine (i.v.) Decrease phase 0 -Ventricular tachycardia -Exacerbation of arrhythmia
-Decrease the duration of & fibrillation post- -SA standstill in pt. w/ MI
the action potential conversion -CNS toxicity @ hi dose
-Block active/inactive Na+ -Arrhythmia ass w/
channel depolarization post Interactions
-Mostly effects MI/digoxin toxicity -Agents enterfering w/ hepatic
ventricle/purkinge (long -Not for long-term perfusion or P450-
plateau) prophylactic post MI
-No affect on K+ (shorten *Not useful in atrial
APD) arrhythmias
Ib Tocainamide Similar to lidocaine Same as lidocaine -Frequent @ therapeutic dose
Mexilitine Orally active -Neurologic: N, tremor, blurred
Ic Flecainide -Suppress phase 0 Purkinje -Life threatening vent -Vent arrhyth
Propafenone and myocardial cells arrhythmias -Dizziness/HA?nausea
Moricizine -Slow dissociation from Na+ -Refractory vent -Visual disturbances
channel in recovery arrhythmias -Increases mortality post-MI tx

II Propranolol Rx’s Decrease Phase 4 -Recovery from MI to Hypotension
(Overload and -Depresses SA-node freq prevent sudden death Aggravation of CHF
re-entry) ==> sinus bradycardia -Control SVT & A-fib Asystole
Acebutol (B1) -Depresses automaticity of -Exercise/stress induced CI – asthma etc
Esmolol (B1) purkinje vent. Arrhythmias
Satolol -Decreased conduction AV-
(Non-sel) node -In ICU give esmolol
-Suppress ectopic (short t ½ IV)
ventricular depolarization
-Hemodynamic activity
III Satolol -Renal excretion Tx/prophylaxis severe -Postural Hypotension
(unchanged) ventricular -Proarrhythmic
-Block K+ channels – prolong tachyarrhythmias -Torsades des pointes
AP-phase 3 -Atrial arrhythmias
-non-selective B-blocker
III Amiodarone Prolongs the AP & ERP -Supraventricular -Pulmonary Fibrosis
- Blocks inactivated Na- Arrhythmia -“Grey man syndrome”
channels (class I) -Ventricular tachycardia Caused by iodine accum in the
-Blocks K+ channels – -Anti-anginal skin
prolong AP -Low dose for atrial -Thyroid disorder
-Mostly effects arrhythmia -Photosensitivity
purkinje/ventricular (long -Corneal depositis
plateau) -Hepatotoxicity
-Variable t ½ 30-120 days – -Thyroid (hi iodide)
steady state when A & DEA
is equal (2 weeks) Drug interaction – digoxin,
warfarin, quinidine, theophylline
IV Verapamil -Blocks L-type Ca++ DOC-Atrial -Negative inotropic effect
Diltiazem channels fibrillation/flutter – -Contraindicated in depressed
Bepridil -Lg effect on AV conduction decrease ventricular cardiac function.
-Re-entry SVT
-Ischemic heart disease
Adenosine -Enhance K+ conductance Hyperpolarization -Flushing, bronchoconstriction
-Inhibits cAMP-mediated -A-fib, V-fib
influx à hyperpolarization
(esp. AV node)
Magnesium -Mech u/k Tx for torsades des
-Fxnal Ca++ antagonist pointes
-Digitalis induced
-Acute MI

Autonomic Control of Heart

Acetylcholine -Increases K+ Current, thus -This is how Vagal -Cholinergic innervation found
hyperpolarizing the cell activity leads to lower only in atrial and nodal cells.
-Decreases L Ca2+ current, heart rate.
thus slowing the action
potential through the nodes.
Norepi -Increases all ion channel -Adrenergic innervation is found
(Epi) currents thus the Action throughout the heart.
Potential duration is -More symp to AV node than
shortened. SA node.

Things u shouldn’t do

Disease Contraindicated Reason

COPD, asthma B-blockers Induction of bronchospasm
ACE-I Induction of cough, use AT1
Bradycardia Clonidine Aggravation, risk of Adams-Stokes
B-blocker syndrome
Diabetes Thiazides Reduced glucose tolerance
B-blockers Blunt sx of hypoglycemia
Gout Thiazides Reduced excrfetion of uric acid
CAD Hydralazine Provocation of angina (reflex
Prazosin tachycardia)
Peripheral artery occlusive disease B-blockers Aggravation/manifestation
CHF Ca++ antagonist Negative inotrope
Renal failure Amiloride, Triamterene May cause hyperkalemia
ACE-I Plasma concentration up, side effects

Sx/problem Approach
Fatigue Rest, + intotrope
Edema Salt restriction
Digitalis (+ inotropre)
Dyspnea Diuretic (thiazide, loop)
Congestion Nitrovasodilator
Poor cardiac + Inotrope, digitalis
Increased ACE-I
preload/afterload Ang-block
Cardiac tissue ACE-I
remodeling Ang-block
Irreversible heart Transplant


Cell wall Penicillin

damage/syntheisis Cephalosporins
inhibited Monobactams
Cytoplasmic Polymyxins
membrane damage or Polyene antibiotics
sythesis inhibited
Inhibit Quinolones (DNA Gyrase)
synthesis/metabolism Rifmapin
of nucleic acids Nitrofuranotoin
Inhibit protein Chloramphenicol
synthesis Tetracyclines
Modify energy Sulfonamide
metabolism Trimethoprim
Nucleic acid analogs Zidovudine

Chemotherapy drugs

Drug Mechanism Clinical Use Side Effects

SULFONAMIDES Sulfisoxazole -W/ phenazopyridine for Nocardia- 1. Hypersensitivity

RAPIDLY ABS. UTI immunocompromised (Stevens-johnson)
Short acting GENERAL: Sulphonamides -- Pneumonia/brain 2. Crystalluria, hematuria
are DOC for PCP infections abcess 3. Hemolytic anemia (G6PD
of AIDS Trachoma def)
Lympphogranuloma 4. Kernicterus
venereum 5. Displacement of drugs from
UTI – e. Coli/proteus binding sites (warfarin,
6. Drug interaction (292
Sulfadiazine -W/ pyrimethamine for Above + toxoplasma in
toxoplasma combo
Intermediate Sulfamethoxoazole -Combo w/ trimethroprim Above + resp. infection in
acting for UTI/resp. tract combo
-Gram –
Long acting Sulfadoxine -Used w/ pyrimethamine Prophylaxis for malaria

POOR Phthalylsulfathiazole -Rx’s bacillary infections Salmonella

ABSORPTION Succinylsulfathiazole -Poor abs. In GI tract Shigella
SPECIAL Sulfacetamide Rx’s the eye Chlamydia trachomatis
PURPOSES probs/conjunctivitis
Sulfasalazine Broken down to 5-ASA IFB

Mafenide Blocks carbonic anhydrase Burns (topical) Irritation

UTI DRUGS Nalidixic acid Inhibit replication by -UTI – gram – -Articular damage (children)
QUINOLONES Norfloxacin inhibiting topoisomerase II -Cutaneous & ST infections -Photosensitivity
Cinoxacin (except nalidixic acid) -GI irritation
Ciprofloxacin -Respiratory –) except -Rash
nalidixic acid) -Convlsions
-Bacterial enteritis N/V
Pseudomonas aerugenosa -May cause increase
intracranial pressure in kids
Ciprofloxacin -Pseudomonase assoc. w/
(Best quinolone) cystic fibrosis
-Enterobacteriacea &
other gram – bacilli
-Synergistic w/ penicillins
-Acute diarrrheal enteric
pathogens (grm – rods)
-UTI’s comp/uncomp

OTHERS Methenamine Liberates formaldehyde w/ -Gastritis
man urinary pH <5.5 -Chemical cystitis
del Metabolite caustic to bugs -Hematuria
ate in urinary system. -Painful/frequent micturition
(Methenamine + -DO NOT GIVE W/
mandelic acid) SULFONAMIDES – insoluble
complex (crystaluria)
Nitrofurantoin -Bacteriostatic UTI’s – E. Coli Interstitial fibrosis
-U/k mechanism Peripheral neuritis
-Turns urine brown Hemolytic anemia G6PD def.
Cholestatic jaundice
GI irritation
Phenazopyridine -Used along w/ urinary -Used to decrease burning -Orange urine
antiseptics piss -Overdosage can produce
CELL WALL Penicillin -Inhibits cell wall synthesis -Strep Hypersensitivity
I (bacteriocidal) -Neisseria Herxheimer rxn (syphilis)
N -Binds PBP (penicillin -Gram + bacilli (clostridium Superinfection
H binding protein) to inhibit diptheria, perfringents, b. Interstitial nephritis
I transpeptidase anthracis) (methicillin) not used now
B -Activates autlytic enzymes -Spirochetes (especially CNS toxicity – convulsions
I -B-lactams synergistic w/ sensitive) Electrolyte imbalance (salts)
T aminoglycosides
Penicillin G -IV or IM Serious life threatening
(Benzyl penicillin) -Orally ineffective disease
-Poor CNS effects (unless
Penicillin V Orally – acid stable Prophylaxis/mild infections

Procaine penicillin Slo abs. Lasts 12-24 hr.s Gonococcal infections

Benzathine penicillin Abs. Very slow lasts 2 wk.s

Usually suppository form
Amoxicillin -Broad spectrum DOC gram + (ampicillin) Pt. w/ mono will develop rash
Ampicillin -Commonly given w/ Beta Gram -
lactamase inhibitors
(sulbactam & clavulinic
Cloxacillin Penicillinase –resistant Methicillin – interstitial
Oxacillin nephritis
Piperacillin Tx of pseudomonas infxn Pseudomonas Carbenicillin & Ticarcillin
Mezlocillin causes platelet dysfxn

CEPHALOSPORINS Cephalosporins Similar to penicillin 1st generation Pain @ injection site
Less susceptible to B- -Gram + Thrombophlebitis
lactamase -Gram – (community acquired) Diarrhea
-3 generations -UTI Nephrotoxicity
-E. Coli
-Klebsiella Produces false + urine test
2nd Generation for glucose
-<Gram +
->Gram – Anti-vit. K effect
-#’S 4-6 of 1st generation -Moxalactam, cefamandole
-h. flu & cefoperazone cause
-Enterobacteriaceae disulfiram –like rxns
1st generation PARENTERAL -Not liphophilic HEN-PEcK
Cefazolin -Don’t cross into CSF H. Flu
Cephalothin Enterobacteriaceae
Cephapirin Neisseria
Cephradine Proteus
ORAL E. Coli
Cephalexin Klebsiella
2nd generation PARENTERAL Enter CSF HEN-PEcK (S)
Cefamandole -Cefuroxime -Serratia
Cefotetan Cefaclor
Cefonicid Biliary excretion
Cefuroxime sodium -Cefaamandole naftate
Cefoxitin Tx B. Fragilis
Ceforanide -Cefotetan disodium
-Cefoxatin sodium
Cefuroxime axetil
3rd generation PARENTERAL CNS – cefotAXime, All penetrate CNS EXCEPT
Cefoperazone ceftriAXone cefoperazone
Ceftriaxone --Think of an AX to the head.

4th generation Cefepine -Extended spetrum Gram – resistant bacillit to
-Increased stability to 3rd generation cephalo’s
SPECIAL Cefamandole – 2gen Eliminated vial biliary
C Cefoperazone – 3 ge For pt.s w/ renal problems
EP Ceftriaxone- 3 gen
Cefamandole – 2gen Cause disulfiram-like rxn w/ Hypoprothrombinemia
Cefoperazone 3 gen alcohol disulfiram-like rxn
Moxalactam – 3 gen

Ceftazidime – 3gen Pseudomonas
-Taz haz pseudomonas so tx
Cefotetan – 2gen All tx B. fragilis b. Fragilis
Cefoxitin – 2 gen
Ceftizoxime – 3gen
Moxalactam – 3gen
OTHERS Cycloserine -Inhibits conversion of L-- 2nd line tx for TB & CNS – psychoses
>D-alanine mycobacteria infxn Delirium
Nocardia infection if Confusion
sulfonamides fail (CNS) H/a
ERYTHROMYCIN Erythromycin Binds 50s -DOC in atypical pneumonia -GI irritation
-Inhibits translocation -Legionella, mycoplasma, -Hypersensitivity –
-No CNS chlamydia cholestatic jaundice (esp.
-Excreted in bile -Campylobacter jejuni w/ estolate salt of
-Alternate in penicillin -Strept/mastoiditis … erythromycin)
resistance penicillin 1st -Inhibit cyt P450 enzymes
Clarithromycin Clarithromycin
Azithromycin -Toxoplasmosis encephalitis,
cryptosporidium diarrhea,
peptic ulcer from H. Pylori
Clindamycin Same Gram + cocci
Resistant flaciparum, vivax
Vancomycin -Inhibits cell wall synthesis SERIOUS staph infections Must be given slowly
- -Oral tx of FONT
pseudomembranous colitis Flushing
- Ototoxic
Metronidazole DOC for amoebic dysentery
-Anaerobes …B. Fragilis
DOC – C. Difficile


Drug type Drug Mechanism Clinical Use Side Effects

PROTEIN Tetracycline -Broad spectrum -BCUM-RATC ADH antagonist

SYNTHESIS -30s Borellia -Fanconi-like syndrome
INHIBITORS -Prevents elongation Chlamydia -GI irritaton
-Impaired abs w/ food Ureaplasma -Pain & phlebitis
-Chelation w/ cations Mycoplasma -Hepatotoxic
-DON’T GIVE W/ Rickettsia -Photosensitivity
PENICILLIN Acne -Superinfection
(antagonist) Tularemia -Hypersensitivity
-All concentrate in Cholera
Spleen, skin, teet etc. Also: bacillary infxn, traveler’s
Gram + resistant, diarrhea, UTI
Chlortetracycline Group I -Chloro more hepatotoxic
Oxytetracycline -Renal & biliary
Demeclocycline Group II SIADH Photosensitivity
Diabetes insipidus
Minocycline -Group III Vestibular toxicity
-Enters CSF w/o
inflamed meninges
-No food interruption
Doxycycline -Group III
-Biliary excretion
Good for renal
-No food interruption
Chloramphenicol -Binds 50s -Broad spectrume Aplastic anemia
-Inhibits peptide bond DOC for salmonella Gray baby syndrome
formation -Brain abcesses Superinfection
-Inhibit peptidyl -Also for all the other nasty little Hypersensitivity
transferase rickettsia, mycoplasma, chlamydia GI – N/V
etc. etc.