ELIMINATION DRUGS

Name Class MOA Side effects Drug Interactions What it helps

“-tidine” H2 Receptor H2RAs decrease gastric acid Malabsorption of iron, -Duodenal and
Antagonist secretion by reversibly binding to calcium, magnesium Gastric Ulcers
histamine H2 receptors located on -GERD
gastric parietal cells, thereby -Heartburn
inhibiting the binding and action of
the endogenous ligand histamine.
H2 blockers thus function as
competitive antagonists.

Ranitidine H2 Receptor Really popular constipation, nausea

Antagonist vomiting, hepatotoxicity
Increases risk of getting
pneumonia
Blood dyscrasias
(neutropenia and
thrombocytopenia)

Cimetidine H2 Receptor Headache, Diarrhea warfarin, phenytoin,

(Tagamet) Antagonist diazepam,
chlormethiazole,
propranolol, lidocaine

Famotidine H2 Receptor confusion, hallucinations,

(Pepcid) Antagonist agitation, lack of energy;

Bradycardia, decreased
respirations

“-prazole” Proton Pump Proton pump inhibitors (PPIs) Malabsorption of: GERD,
Inhibitor block the gastric H,K-ATPase, iron, calcium, Duodenal/Gastric
-Taken 30 inhibiting gastric acid secretion. magnesium ulcers
mins. before malabsorption PUD
meals They are the most potent
inhibitors of acid secretion
available today.
Omeprazole PPI Back, leg, or stomach Oral Iron, Part of the treatment
pain. iazepam, for PUD
carbamazepine,
clozapine, indinavir,
nelfinavir,

Iansoprazole PPI dizziness, decreases stomach

(Prevacid) fast or irregular heart rate, acid, so it may
watery or bloody diarrhea, change how well
muscle cramps or these products work.
weakness,

Pantoprazole PPI Headache, diarrhea

Antacids alkaline agents, not recommended Increases stomach OTC acid reflux
as only treatment, symptom releif PH, so affects how relief.
only! OTC Iron, Calcium and
Magnesium
absorption

Aluminum Antacid Constipation

Hydroxide

Milk of Antacid Diarrhea

Magnesia
(Magensium
Hydrxide)

Calcium Antacid
Carbonate

Sucralfate Reacts with hydrochloric acid in

the stomach to form an adherent,
paste-like substance capable of
acting as an acid buffer

All a bit Antidiarrheal Agonists, Targets MU2 receptors Low doses otc, high prevents or relieves
different s (opioids in GI, causes decreased doses prescription diarrhea; inhibits
 +atropine) peristalsis. The Atropine blocks peristalsis and
parasympathetic system and reduces fecal volume
stimulates the sympathetic
drive/stimulation- in the gi tract,
this decreases motility, which we
are working for.
Combats CNS depression and
decreased heartrate/ventrility
drive
Atropine is a stimulant, which
countereffects the opioid!

Lomotil Antidiarrheal
(dypenoxylat
e opioid +
atropine)

Imodium Antidiarrheal
(loperamide
HCL
meperidine +
atropine)

Metamucil, Bulk Forming Pull water into stool and add size Dehydration
PO, Laxative to it, water intake a must, used in
Suppository long term care homes

Colace Softener Pull water and Fat into Stool, Systemic effect, patients Post myocardial
(Docusate decrease surface tension and need to have good renal infarction (less strain)
Sodium) emulsify stool function for excretion Post surgery

Milk of Saline/ Pull water into stool Lactulose not absorbed in Pre-procedural
Magnesia, Osmotic lactose intolerance, milk
Lactulose of magnesia is renally Potent
excreted, so good function
 needed.

Dulcolax, Stimulants Irritants, increase peristalsis, not N&V, cramping DO NOT USE IF
Senna, first choice for constipation or pre OBSTRUCTION OF
Castor OIl surgery PERFORATION

MIneral Oil, Lubricating Lubricates the anus for smooth

Glycerine, sailing
PR (rectal
injected)

H1 Reduces vestibular excitation motion induced,

Antagonists morning sickness,
anticipatory nausea

Dimenhydrin H1
ate Antagonist

Meclizine H1
(dramamine) antagonist

Doxylamine+ H1
pyridozine antagonist
hydrochloride
(diclectin)

Ginger Increases intestinal peristalsis, Safe in moderate doses,

Gravol increasing emptying of the but if overdose, bleeding,
stomach instead of vomiting, CNS depression
decreasing the sensation of
nausea.
-Antiplatelet

Scopolamine Anticholinergi Dry mouth, constipation, Motion sickness,

(hyoscine) c/ •(Ach block) urinary retention N+V
-transdermal Antimuscarini •Crosses BBB (in CNS)
patch c •Misuse:
(Belladonna •Dilated pupils,
plant; blurred vision,
Brugmansia increased sensitivity
tree) to light
•Confusion
•High doses:
amnesia, sedation,
unconsciousness

Ondasetron 5HT3 Serotonin receptor Antagonist -Known to prolong the QT Drug induced,
(Zofran) Serotonin interval. Chemotherapy,
-Po, IV Antagonist -May cause cardiac Visceral pain
dysrhythmias. Nausea, chronic pain

D2 Receptor Stimulates GI motility Uses for NJ tubes

Antagonist, because it allows the
Phenothiazin stomach and GI tube
es to become large
enough, relaxed
enough. No vomiting
in between

Metocloprami D2 Receptor
de (maxeran, Antagonist
Reglan)

Prochlorpera D2 Receptor Crosses BBB and causes

zine, Antagonist sedation
Prescription
only, PO, IV

Dronabinol, Cb1/2 Receptor binding stimulated Patients may feel a little Chemotherapy,
Cesamet Agonism GABA, inhibitory effects, inhibition more sedated Chronic Disease,
of sympathetic activity (therefore Challening cases
no nausea) (Nausea)

PERFUSION DRUGS
Name Class MOA Side Effects Drug Interactions What it helps
Nipride Direct Acting Stimulates endothelial cell- Reflex tachycardia, Hypertensive Crisis
(Nitroprusside) - Vasodilator produced endogenous hypotension, syncope,
IV t1/2= 2 substance NITRIC OXIDE headache.
minutes (IV (L-arginine activates nitric
infusion) OR ET oxide)
for pulmonary
vasodilation.

Hydralazine- Direct Acting Stimulates endothelial cell- Reflex tachycardia, Hypertensive Crisis
PO/IV Vasodilator produced endogenous hypotension, syncope,
substance NITRIC OXIDE headache
(L-arginine activates nitric
oxide)

Furosemide Diuretics Blocks Na+, K+, Cl- (NKCC2) Hypokalemia, ototoxicity Highly PPB *1st line therapy for
(Lasix)- Potent, (Loop) reabsorption in Loop of Henle - hypertension
PO/IV increased Na, K, Cl out

Hydrochlorothia Diuretics -Renal distal convoluted tubule hypokalemia, *1st line therapy for
Thiazides increase
zide (HZTZ)- (Thiazides) -Decreases reabsorption of Na hyponatremia, hypertension
digitalis levels
PO from distal tubule hyperglycemia promoting visual
-alcohol and caffeine can
-increased Na & K out (allows disturbances.
enhance the hypotensive
K out) effect of Thiazides.
-ADME travel unchanged

Chlorothiazide Diuretics -Renal distal convoluted tubule hypokalemia, *1st line therapy for
Thiazides increase
(Diuril)- PO (Thiazides) -Decreases reabsorption of Na hyponatremia, hypertension
digitalis levels
from distal tubule hyperglycemia promoting visual
-alcohol and caffeine can
-increased Na & K out (allows disturbances
enhance the hypotensive
K out) effect of thiazides.
-ADME travel unchanged

Metolazone Diuretics -Renal distal convoluted tubule hypokalemia, *1st line therapy for
Thiazides increase
(Zaroxolyn)- PO (Thiazides) -Decreases reabsorption of Na hyponatremia, hypertension
digitalis levels
from distal tubule hyperglycemia promoting visual
-alcohol and caffeine can
-increased Na & K out (allows disturbances
enhance the hypotensive
 K out) effect of thiazides.
-ADME travel unchanged

Spironolactone Diuretics -In Distal tubule. Hyperkalemia- can cause DON’T give with *1st line therapy for
(Aldactone)- (Potassium a Myocardial Infarction ACE inhibitors or hypertension
long t1/2= 1-2 Sparing) -Blocks renal aldosterone ARBs because of
days (Aldosterone = causes Na hyperkalemia.
retention) -Receptors = DON’T give with
increases Na out & keeps K+ in Digoxin.
-increases Na out
-ADME:
Therapeutically active
metabolites

Aldactazide- PO Thiazide and -Used very frequently Excellent

Potassium maintenance therapy
Sparing combo -Balances out K+ for Hypertension

Mannitol Diuretics -Proximal tubule & Loop of -Cross BBB = tx of:

(Osmitrol) (Osmotic) Henle
-monitor BP Cerebral edema
-Osmotic increase of Na & H20
and LOC Intraocular
losses & inhibits ‘Renin’ hypertension
release
•call for tissue
entrapped fluid to be
drawn into
circulation.

-Temporary measure
for treatment of
intraocular pressure
-low use for
cardiovascular

Isosorbide Diuretics -Proximal tubule & Loop of -Cross BBB = tx of:

 (Osmotic) Henle Cerebral edema
-monitor BP
-Osmotic increase of Na & H20 Intraocular
and LOC
losses & inhibits ‘Renin’ hypertension
release
•call for tissue
entrapped fluid to be
drawn into
circulation.

-Temporary measure
for treatment of
intraocular pressure
-low use for
cardiovascular

“-pril” ACE Inhibitors Reduce vasoconstriction Severe hypotension *1st line therapy for
(vasodilate) via Angiotensin- Heart Failure
converting enzyme HIGH EFFICACY
Hypertension

Enalapril
(Vasotec)

Captopril-
frequently used!

Monopril

Ramipril
(Altace)

Losartan ARBs Angiotensin II receptors Hypotension Hypertension and

(Cozaar) blocked in smooth & cardiac Heart Failure
muscle & kidneys & adrenal -They take a few
gland weeks to have an
effect.

Ibesartan ARBs Angiotensin II receptors Hypotension Hypertension and

(Avapro) blocked in smooth & cardiac Heart Failure
muscle & kidneys & adrenal -They take a few
gland weeks to have an
effect.

Hyazaar HCT Thiazide

Diuretic and
ARB combo

Cosart-H Thiazide
Diuretic and
ARB combo

Calcium ↓ heart rate (cardiac muscles.) -Dizziness, flushing,

Channel ↓ cardiac output (cardio-s.) hypotension
Blockers
-optimize cardiac contractions -Reflex tachycardia
↓ blood pressure and vasodilation
(smooth muscles.) -Peripheral edema
-Dysrhythmias
-Exacerbation of heart
failure

Nifedipine Calcium Muscle contraction regulated Angina and

(Adalat) Channel by calcium (Ca 2+ enters cell = Hypertension
Blockers contraction initiated)
-Ca 2+ influx blocked =
smooth muscle relaxation
-Specificity: vascular-selective
smooth muscle.

Amlodipine Calcium Muscle contraction regulated Angina and

(Norvasc) Channel by calcium (Ca 2+ enters cell = Hypertension
Blockers contraction initiated)
-Ca 2+ influx blocked =
 smooth muscle relaxation
-Specificity: vascular-selective
smooth muscle.

Verapamil Calcium Muscle contraction regulated Arrhythmias-

(Isoptin) Channel by calcium (Ca 2+ enters cell = specifically Atrial
Blockers contraction initiated) Fibrillation
-Ca 2+ influx blocked =
smooth muscle relaxation
-Specificity: cardio-selective
(myocardial cells.)

Diltiazem Calcium Muscle contraction regulated Arrhythmias-

(Cardizem) Channel by calcium (Ca 2+ enters cell = specifically Atrial
Blockers contraction initiated) Fibrillation
-Ca 2+ influx blocked =
smooth muscle relaxation
-Specificity: cardio-selective
(myocardial cells.)

GINSENG Herbal Calcium Channel antagonist Can cause some

Dose: 20-30 drug-drug
mg/day interactions

“-ol” Beta Blockers Bradycardia, lethargy, GI Reduces mortality in

*The client disturbance, congestive heart failure
may not notice Blocks Beta1 or Beta2- heart failure, hypotension,
blocking endogenous
significant catecholamine (NE, E). depression.
improvement
during early
therapy

Atenolol Beta Blockers Vasodilation Hypertension,

(Beta1) Angina, and
Arrhythmias

Propranolol Beta Blockers Antiarrhythmic (<AV node) Arrhythmias

Extensive First (Beta1 and
Pass Beta2)
Metabolism

Metoprolol Beta Blockers Angina and

(Beta1, high Hypertension
doses=Beta2)

Prazosin Alpha Blockers Peripheral vasodilation Hypertension,

(Alpha 1) symptoms of an
enlarged prostate,
and PTSD.

Phentolamine Alpha Blockers Peripheral vasodilation Controls paroxysmal

(Unselective hypertension
alpha) resulting from
anesthesia, stress, or
operative
manipulation of a
tumor.

Lopressor HCT Thiazide and

Adrenergic
Antagonist
combo

Lovastatin Statins Lowers LDL myopathy- weakening of CYP3A4, CYP2C9 *1st line for post
(Mevacor)- PO -Decreased synthesis (via muscles interactions Myocardial Infarction
qd HMG reductase inhibition) & Pregnancy category X- Highly PPB
-liver function increased hepatic metabolism interferes with fetal CNS
dependant myelination
Rhabdomyolysis

Atorvastatin Statins Lowers LDL myopathy- weakening of CYP3A4, CYP2C9 *1st line for post
(Lipitor)- PO qd -Decreased synthesis (via muscles interactions Myocardial Infarction
-liver function HMG reductase inhibition) & Pregnancy category X- Highly PPB
dependant increased hepatic metabolism interferes with fetal CNS
myelination
Rhabdomyolysis
Simvastatin Statins Lowers LDL myopathy- weakening of CYP3A4, CYP2C9 *1st line for post
(Zocor)- PO qd -Decreased synthesis (via muscles interactions Myocardial Infarction
-liver function HMG reductase inhibition) & Pregnancy category X- Highly PPB
dependant increased hepatic metabolism interferes with fetal CNS
myelination
Rhabdomyolysis

Niacin- a form of Herbal Increases HDL -Intense flushing and hot Ideal for patients with
Vitamin B3 flashes low HDL
-decreases liver cholesterol
- 3 g/day synthesis and increases -Tingling of the fingers -Used for synergy
clearance and toes with Statins mainly

Fenofibrate Fibrates Decreases VLDL -Used for synergy

(Lipidil) with Statins mainly
-increases lipolysis and
metabolism

Acetylsalicylic Antiplatelet Aspirin OD Treats acute event

Acid (Aspirin)- NSAIDS Block Thromboxane A2 in -activated charcoal and for routine
Zero Order Non-selective degranulation -sodium bicarbonate prevention
Elimination COX Inhibition -ASA: + COX 1 inhibition = -hemodialysis
‘Baby’ Aspirin- decreased platelet aggregation -NO antidote Low-dose
antiplatelet and increased chance of -close monitoring antithrombotic
activity happens bleeding Reye’s Syndrome (cardiac treatment)
before the First -contraindicated in Low-moderate joint
Pass Effect children. pain
-Recommended -causes fulminant
dose for hepatitis and cerebral
pain/inflammatio edema.
n: 325-650 mg -can be fatal.
q4h To treat: alkalinize urine to
-Recommended help excrete Aspirin.
dose
Cardiovascular:
81 mg
-Pediatric: not
recommended
10-15mg/kg if
indicated for
Kawasaki
Syndrome-
trigger=viral
infection

Dipyridamole Antiplatelet Treats acute event

Block Thromboxane A2 in and for routine
degranulation prevention

Aggrenox Aspirin and

Dipyridamole
combo

Clopidogrel Antiplatelet Treats acute event

(Plavix) Block ADP in degranulatio = and for routine
decreased platelet adhesion prevention
Great for children
(can’t take Aspirin)

Abciximab Antiplatelet Used pre/during

(Reopro)- IV Glycoprotein IIb/IIIa receptor
interventions to
bolus inhibition = decreased fibrin-
remove obstruction
(continuous receptor binding
infusion)
Short-term use
EXTREMELY
POTENT

Integrilin- IV Antiplatelet Used pre/during

bolus Glycoprotein IIb/IIIa receptor
interventions to
(continuous inhibition = decreased fibrin-
remove obstruction
infusion) receptor binding
Short-term use
EXTREMELY
POTENT

Aggrastat- IV Antiplatelet Used pre/during

bolus Glycoprotein IIb/IIIa receptor
interventions to
inhibition = decreased fibrin-
(continuous remove obstruction
infusion) receptor binding
Short-term use
EXTREMELY
POTENT

Heparin Anticoagulant High risk patient for

1st line pre- *When Inhibit Thrombin = no fibrin! Heparin Induced clotting i.e.
surgery brushing teeth, Thrombocytopenia - dysrhythmias,
Lab monitoring= use a soft Immune reaction to complex surgery;
heparin (& platelet factor severe MI
activated partial toothbrush 4) = activation of thrombin
thromboplastin *Avoid flossing = disseminated
time (aPTT) *Hold direct coagulation
pressure on
any puncture -incidence= upto 50% of
site for 15 patients
mins.
*Ginger, garlic, -life-threatening= up to 3%
of patients
and green tea
may increase
the risk of
bleeding
*Contraindicat
ed in clients
with gastritis
(increased risk
of bleeding)
Enoxaparin Anticoagulant High risk patient for
(Lovenox)- (Low- Heparin Induced clotting i.e.
Subcutaneous molecular- Thrombocytopenia - dysrhythmias,
injection weight Immune reaction to complex surgery;
heparin (& platelet factor severe MI
Low potency! Heparins) 4) = activation of thrombin
Lab = disseminated
monitoring= coagulation
Anti Factor XA
levels -incidence= upto 50% of
patients

-life-threatening= up to 3%
of patients

Dalteparin Anticoagulant High risk patient for

(Fragmin)- (Low- Heparin Induced clotting i.e.
Subcutaneous molecular- Thrombocytopenia - dysrhythmias,
Immune reaction to complex surgery;
injection weight
heparin (& platelet factor severe MI
Low potency! Heparins) 4) = activation of thrombin
Lab = disseminated
monitoring= coagulation
Anti Factor XA
levels -incidence= upto 50% of
patients

-life-threatening= up to 3%
of patients

Dabigatran Anticoagulant Stroke prevention

(Pradaxa)- Lab Block Thrombin receptors &
prodrug monitoring= factor Iia- Thrombin
activated
partial
thromboplastin
time (aPTT)
Warfarin Anticoagulant Highly PPB High risk patient for
(Coumadin)- Lab Inhibit hepatic formation of Narrow TI clotting i.e.
PO, long t1/2 monitoring= specific clotting factors (II, VII, dysrhythmias,
Prothrombin IX, X) complex surgery;
severe MI
time (PT/INR)

Alteplase- IV Thrombolytic Treats Acute Event

t1/2= 13-16 Based on endogenous clotting (post-clot formation=
minutes control: Plasmin (dissolves clot lysis)
fibrin clot)
-Plasminogen (inactive) in
bloodstream, Tissue
plasminogen activator (tPA)
converts to Plasmin => clot
lysis

Reteplase- IV Thrombolytic Treats Acute Event

t1/2= 13-16 Based on endogenous clotting (post-clot formation=
minutes control: Plasmin (dissolves clot lysis)
fibrin clot)
-Plasminogen (inactive) in
bloodstream, Tissue
plasminogen activator (tPA)
converts to Plasmin => clot
lysis

Nitroglycerine Organic
(Nitro)- SL Nitrates Exogenous ‘Nitric Oxide’ - Can cause fainting, *1st line Acute
tablet/spray/ IV Causes vasodilation dizziness- especially in Intervention
-1 SL tablet older adults
q5min x 3 doses
=> call EMS -Should be sitting down
while taking nitroglycerine
-High coronary
circulation
efficacy
Topical
ointment= can
be applied to
ANY skin
surface
Patch=
repeated use of
the SAME
application site
will decrease
absorption and
cause skin
irritation.
Isosorbide

Digoxin Cardiac -affects the overall electrolyte Narrow therapeutic index

(Lanoxin)- PO/ Glycosides- •Monitor: HR (apical Arrhythmias
transport across cell = close monitoring
IV Known for P x 1 minute!), ECG
membrane:
Digitoxin- PO/IV 2000 yrs •Digitalization (loading , monitor
•Blocks Na/K ATPase = blocks dose) electrolytes!
-Plant extract exit of Na (3 out is normal) =
from Digitalis •& serum levels ongoing •toxicity: N&V 1st
high Na in cell activates Na/Ca prior to next dose sign of toxicity
exchanger = increased Ca in = (antidote: Digibind)
increased contractility!
toxicity= visual
•Slows electric conduction disturbances
pathway at AV node
-Increased contractility via
overall increase of Ca++ in cell
-Decreased HR via slowing of
nodal transmission = increased
CO

“-none” P Inhibitors •Monitor: ECG, BP,

•Block enzyme Acute Congestive
HR
Phosphodiesterase (PDE) => Heart Failure (short
increase cAMP activity term treatment)
-Increased contractility in
myocardial cells
-Vasodilation
•Inhibition of
phosphodiesterase in
 endothelial cells

P Inhibitors
Milrinone-

onset = 2
minutes
•IV only

Amrinone-

onset = 2
minutes
•IV only

Vagra P Inhibitors CYP3A4 Drug-drug

(Sildenafil) Specific to PDE5 High doses can lead to a interactions. Erectile dysfunction
MI.
Leads to accumulation of blood
flow in the erectile tissue,
causing a sustained erection.

Dobutamine- Adrenergic •Direct sympathomimetic: •Monitor:

short t1/2, Agonists continuous Moderate to severe
continuous IV •Beta 1 specific! pain
monitoring of VS;
infusion •Some B2 binding- lower angina,
affinity tachycardia, ECG
(arrhythmias)

Dopamine HCL- Adrenergic •Precursor to Norepinephrine, •Monitor:

short t1/2, Agonists stimulates catecholamines: continuous Hypotension, Low
continuous IV monitoring of VS; CO
Non-selective Beta
infusion angina,
•Increase contractility tachycardia, ECG
•Increase cardiac output (arrhythmias)

•Some vasodilation due to

 dopamine receptors (in smooth
muscle + in renal beds) =
increased renal perfusion

Clonidine- Alpha2 Stimulate (agonise) CNS alpha

PO/IV Agonists 2 receptors in vasomotor Orthostatic Hypotension, Resistant
PRODRUG center directly = decreased Headache Hypertension
presynaptic Ca2+ levels =
inhibiting release of
norepinephrine (NE)
NEGATIVE FEEDBACK LOOP
= net effect is decreased
sympathetic tone

Methyldopa- Alpha2 Stimulate (agonise) CNS alpha

PO/IV Agonists 2 receptors in vasomotor Orthostatic Hypotension, Resistant
PRODRUG center directly = decreased Headache Hypertension
presynaptic Ca2+ levels =
inhibiting release of
norepinephrine (NE)
NEGATIVE FEEDBACK LOOP
= net effect is decreased
sympathetic tone

ANTIINFECTIVE DRUGS
Cell Wall Inhibitors
Name Class MOA Side Effects Drug What it helps
interactions

“cillin” Penicillins Gram + bacteria, pharyngitis,

Bactericidal: strep. P, Otitis Media (s.
Penicillin kills bacteria through binding of the pneumoniae)
beta-lactam ring to DD-transpeptidase,
inhibiting its cross-linking activity and
preventing new cell wall formation. Without a
cell wall, a bacterial cell is vulnerable to
outside water and molecular pressures, and
 quickly dies

Pen G (IV) Penicillin Narrow spectrum

Pen V (PO) Penicillin Narrow Spectrum 1st choice now: Pharyngitis

Strep. Pyogenes (Gram +)

Cloxacillin Penicillin Narrow spectrum

Amoxicillin Penicillin Broad spectrum 1st choice now: Otitis Media S.

pneumoniae; Hib; Moraxella

Ampicillin Penicillin Broad spectrum

Pipercillin Penicillin Very broad spectrum

Carbenicillin Penicillin Very broad spectrum

Ticarcillin Penicillin Very broad spectrum

“cillin” Clavulanic Beta lactamase inhibitors

Acid &
tazobactam
(combinatio
n)

Amoxicillin (co- Clavulanic

amoxiclav Acid &
(Augmentin)) tazobactam
(combinatio
n)

Clavulanic
Ticarcillin (co- Acid &
ticarclav tazobactam
(Timentin)) (combinatio
n

Pip-Taz Clavulanic
(Pipercillin/Tazo Acid &
bactam, tazobactam
(Tazosin, (combinatio
Zosyn)) n
Broad spectrum
penicillin

Ampicillin/ Prophylaxis
subactam

Piperacillin/ Prophylaxis
tazobactam

“cef” Cephalospo Largest antibiotic class, Chemical structure: 1st choice now for Skin
rins beta-lactam ring Bactericidal infections
gram + and gram -, higher generations cross
BBB (3-5th)

Cefazolin Cephalospo
(Ancef), IV rins

Cephalexin Cephalospo
(Keflex) PO rins

Cefuroxime Cephalospo
rins

Ceftriaxone (3rd High Cross BBB

generation generation
Cephalosporin- cephalospo
E. coli efficacy rins
), Ceftazidine,
Ceftaroline

“-penem” Carbapene Chemical Structure: Beta lactam ring, Very broad spectrum, serious
Imipenum, ms Bactericidal and mixed infections,
Meropenem meningitis, aspiration
Potent, not 1st pneumonia
line therapy; IV
 only Resistance
growing

Polysporin Bacitracin Gram +, broad spectrum,

Prophylactic! topical, ophthalmic, ear prep.
Conjunctivitis, skin/ soft tissue
topical infections

Vancomycin Glycopeptid
e 1st choice now for: MRSA
(Staph. Aureus)

2nd tx for: C.difficile

Daptomycin Cyclic Lipophilic tail

IV Lipopeptide VRSA
Depolarizes cell
Arrest of DNA/RNA/protein synthesis

Protein Synthesis Inhibition Drugs

Name Class MOA Side effects Drug What it helps
interactions

“-ycline” Tetracycline Broad spectrum Gram Bone deformations i.e. Lyme disease, Cholera, H-pylori,
+, -, bacteriostatic Chlamydia, Acne (Accutane preferred:
Vitamin A); Malaria prophylaxis

Doxycycline Tetracycline

Demeclocyclin Tetracycline
e

Tigecycline Tetracycline IV route

VRSA tx

“-mycin” Macrolides PO, very effective, 1st choice now ‘community acquired’
 bacteriocidial, adult pneumonia
bacteristatic, gram + • Last tx option for Gonorrhea
mostly, some - (combined w a Cephalosporin)

Erythromycin, Macrolide

Azithromycin Macrolide
(Zithromax)

Clarithromycin Macrolide
(Biaxin)

Gentamicin -IV Aminoglycosi Gram - POTENT Narrow TI-Serum Gram -, high risk infections
des levels completed!
Tobramycin - Nephrotoxicity, Eye drops for conjunctivitis
ophthalmic Neurotoxicity,
drops Hepatotoxicity

Streptomycin- Aminoglycosi
IV des

Neomycin-IV Aminoglycosi
de

Clindamycin, Lincosamide Serious GI infections (anaerobic)

IV s Skin infections
Surgical prophylaxis (esp. patients with
allergy)

Cefazolin IV + Combination
Gentamicin IV therapy:
• E.g. utilizing
penicillins or properties of
cephalosporins individual
+ drugs to
aminoglycosid improve
es efficacy
Bacterial wall
inhibition +
 bacteriostatic
within cell

RNA DNA TRANSCRIPTION INHIBITION

Name Class MOA Side effects Drug How does it help
interactions

“xacin” Fluroquinolones Many Gi infections, UTI

generations,
gram - ,

Ciprofloxacin 3rd gen Bactericidal

Fluroquinolones

Levofloxacin Fluroquinolones

Norfloxacin Fluroquinoles

Metronidazole (flagyl) Metronidazole (flagyl) Inhibits dna C. difficile (1st choice)

synthesis H.Pylori
Anti protozal Prophylaxis
agent (eg. dental procedures)

ANTIMETABOLITE
Name Class MOa Side effects Drug How it helps
intera
ction
s

-Sulfa prefix Sulfonamides Inhibit folic acid synthesis ,inhibits ALLERGY Gram + & - bacteria
sulfamethoxazole; cellular function UTI (now preferred)
t-
sulfamethoxazole
(TMP/SMX,
Bactrim, Septra)

•Amphotericin – Polyene Fungal Increase cell membrane permeability Fungal infections

1st choice of Antibiotics (Cryptococcus,
therapy Candida,
IV Aspergillus)
•Nystatin
– Candida (skin,
GI infections)
PO

Rifampin TB
+ 4 more anti-TB Treatment 6-12
meds months Resistant
strains present!

•Acyclovir (PO, Herpes Simplex 1 &

IV, cream) 2

•Ganciclovir Herpesvirus-5
(CMV)

Tamiflu Influenza

Amantadine Influenza

Fentanyl Opioids= Centrally •CNS depression = Analgesia

Acting Analgesia sedation,
-inhibits
decreased RR &
substance P ‘Mu’ receptor agonist HR BP & LOC,
-crosses BBB HIGH EFFICACY pupillary
hydromorphone constriction
(Dilaudid), Heroin- AKA smack, •N&V
oxymorphone junk, H., horse, dragon,
(Numorphan), •Pruritus
meperidine black tar, brown sugar
•Constipation
(Demerol),
•IV, inhaled, snorted, •Urinary retention
Morphine,
smoked
methadone •Euphoria
(Metadol), •Highly lipophilic,
Tramadol (Ultram) crosses BBB rapidly
 and Opium= Opioids HOLD opioids if
resp.rate <12/min

•Check for
ALLERGY (Opioid
allergies are not
uncommon)

•Caution: in severe
asthma patients (d/t
opioid stimulated
histamine release)
Pregnancy
Category D

hydrocodone, Opioids
oxycodone MODERATE EFFICACY
(OxyNeo) + Heroin, Opium= Opioids
oxycontin;
Percocet
(oxycodone +
acetaminophen),
Percodan
(oxycodone +
ASA), Vicodin
(hydrocodone +
acetaminophen),
Tramacet
(Tramadol +
acetaminophen),
buprenorphine

Codeine, Tylenol Opioids

#1-#4 LOW EFFICACY
(acetaminophen + Heroin, Opium= Opioids
codeine +
caffeine)

Dicyclomine Muscarinic Antagonist GI smooth muscle relaxant

(Bentyl)

Morphine Opioid Decreased vasoconstriction (decreased MI pain

BP & CO)

Fentanyl AKA Opioid

friend, jackpot,
green
beans/beans,
green
apples/apples,
greenies, eighties,
fake oxy
•High efficacy &
extremely high
potency !!!
Form- often green
pill
•PO, snorted, IV,
SL (blotter paper)
•Laced into other
drugs (cheap!)
Carfentanil- opioid
used as an
elephant
tranquilizer
Fake 80s-
fentanyl posing as
OxyContin

Naloxone Opioid Overdose

(Narcan)
•onset – 2-4
minutes
•Duration of
action = 45 min
•t1/2 60-90 min !

•IM (0.4 mg)

Naltrexone Opioid Dependency

(ReVia)

NSAIDS Other brands NOT 1st Line

Celecoxib Selective COX-2 Therapy Analgesic
removed from
(Celebrex ®) Inhibitor market due to
Rx only (except cardiovascular
topical creams) related
complications
including premature
death (e.g. Vioxx)
•‘black box’ CV
warning

•Ibuprofen (Advil, NSAIDS Ibuprofen-

Motrin) Non-selective COX •headache/1st in
Inhibition migraine protocol
•Ibuprofen-like: (=>’Triptans’)
•Diclofenac •soft tissue swelling
(Voltaren) (tx of sprains)
•Naproxen (Aleve, Indomethacin
Naprosyn)
•Moderate-severe
•Ketorolac joint pain
(Toradol)
•(tx of Arthritis;
•Indomethacin Gout)
(20xASA potency)
= Rx only

Glucocorticoids •Lipophilic = hydrophilic via metabolism

•Short acting: High Efficacy •Joint pain
•Hydrocortisone, -easily excreted (Cortisone injection)
Cortisone, •Overall highly PPB
Prednisone •Anaphylaxis
(Prodrug), •Histamine release suppression •Stabilization of
Prednisolone, •Prostaglandin synthesis inhibition patient post
Methylprednisolon (COX-2) anaphylactic shock
e
•Suppression of (Prednisolone IV,
PO/IV Phagocytes/lymphocytes followed by PO
Prednisone x 3
days)

Glucocorticoids •Lipophilic = hydrophilic via metabolism

•Long acting: High Efficacy •Inflammation
-easily excreted
•Dexamethasone •Autoimmune: e.g.
•Overall highly PPB IBD, Lupus
•(PO, low dose,
daily) •Histamine release suppression •not sole therapy;
used as adjunct
•Prostaglandin synthesis inhibition
(COX-2)
•Suppression of
Phagocytes/lymphocytes

Budesonide Glucocorticoids •Lipophilic = hydrophilic via metabolism •Few side-effects •For Allergic Rhinitis
(Rhinocort) High Efficacy (low systemically) (nasal symptoms)
-easily excreted
Fluticasone •Overall highly PPB
(Flonase)
•Histamine release suppression
Mometasone
(Nasonex) •Prostaglandin synthesis inhibition
(COX-2)
•Intranasal
administration •Suppression of
Phagocytes/lymphocytes

Pulmicort Glucocorticoids •Lipophilic = hydrophilic via metabolism Asthma

(Budesonide), High Efficacy
-easily excreted
Qvar
(Beclomethasone) •Overall highly PPB
 , Flovent •Histamine release suppression
(Fluticasone) •Prostaglandin synthesis inhibition
•Inhalation (COX-2)
administration •Suppression of
Phagocytes/lymphocytes

Diabetes Drugs
Name Class MOA Side effects Drug What it helps
Interactions

Rapid Acting •Ideal for: meal-time bolus; pt eats DM 1

Humalog (Lispro), Novorapid Insulin right away! (food tray ready!!!); in
(Aspart), Apidra (Glulisine)
 insulin pumps; not IV
•Onset: 10-15 minutes

•Peak: 1-2 hr

•Duration: 3-5 hrs

Fiasp (Aspart) – onset: 4 min

-improved mealtime control;
admin. immediately prior or
during meal

Long Acting •Ideal for: background; admin. 1-2 DM 1

•Levemir (Detemir)-smaller
doses do have smaller
duration! Lantus (Glargine)
•Onset: 90 min
Insulin x daily; MUST have separate
syringe for injection
(contamination decreases
efficacy); never IV

•Plateaus for: upto 24 hrs

Tresiba (Degludec) – ultra-long

acting (>30 hrs)

Short Acting •Ideal for: meals (must be 30-45 DM 1

Novolin/Toronto; Humulin R
•Onset: 30 minutes
•Peak: 2-3 hr
•Duration: 6.5 hrs (dose
dependent!)
Insulin= min pre-meal!) BUT issues with
‘Regular’ hypoglycemia & balancing dose w
intake; pt eats!!!
•used IV if ketoacidosis, new dx,
….

Entuzity (KwikPen)
•5x more concentrated; for
high daily insulin
requirements;duration= 15 min
– 20 hrs!!!

Intermediate •Ideal for: background DM 1

Humulin N; Novolin / NPH Acting Insulin replacement, admin. 1-2x daily; if

•Onset: 1-3 hrs
•Peak: 5-8 hrs
•Duration: upto 18 hrs (dose
dependent!)
•Humalog mix 25 = 25%
rapid/75% long
•Humalog mix 50 = 50%
rapid/50% intermediate
•NovoMix 30 = 30% rapid/70%
long
Metformin (Glucophage)
PO, IV available
onset 2-3 hrs
peak 10-16 hrs
Canagliflozin (Invokana)
Glyburide (DiaBeta)
•Action: onset 1 hr, peak 2-3
hrs, duration 10-24 hrs
pt on steroids (can match sugar
peaks; monitor for night
hypoglycemia!!! (evening snack
important); never IV
Pre-mixed DM 1
insulin
formulations
Biguanides Reduces GI glucose absorption DM 2 1st line
Assess liver fx !!! (d/t Drug-drug tx*
Increases cell Glucose uptake & mechanism of interactions
Insulin release action); renal fx check!
assess= metformin
•Dynamics: in GI tract = increased excreted unchanged.
metabolism therefore decreased Adverse effect= lactic
absorption; at cellular level = acidosis
alters mitochondrial activity
SGLT2 increase glucose diuresis less hypoglycemia d/t DM 2
inhibitors no Insulin interaction;
•SGLT2 = transporter of glucose diuresis!; assess
in proximal nephron tubule, renal fx!
increasing glucose reabsorption
by the kidney
•Inhibition = decreases glucose
uptake, and increases glucose in
urine
SULFONYLU Increase Insulin release & Safe for most DM 2
REAS receptor sensitivity diabetic patients; s/e:
weight gain!;
abdominal pain; no
•Administer: PO, daily
Dulaglutide (Trulicity) (SC
injection)
Rosiglitazone (Avandia)
Glucovance
•Glyburide (5 mg) & Metformin
(500 mg)
•Other doses available
Levothyroxine (Synthroid)
-Synthetic form of T4
Onset of action 3-5 days
t1/2 = 6-7 days
Renal excretion
ETOH intake
Incretin =>stimulate insulin release Contraindicated in DM 2
enhancers patients with
•Hormone: Incretin (GLP-1, GIP) pancreatic issues
•Released from small intestine w
food ingestion = stimulates Insulin
release from Pancreas
•degraded by DPP-4 (dipeptidyl
peptidase)
•Mimic Incretin action = Insulin
release from Beta cells
DM 2
-increases glucose uptake into weight gain
cells from plasma
Glyburide •Glyburide – increased Insulin DM 2
and release
Metformin
combo •Metformin – decreased glucose
Hypothyroidism
Therapeutic action = Identical to
endogenous thyroid hormones.
-PO (IV if necessary); 40-80%
bioavailability
-qd (on empty stomach!); GI
absorption
-hepatic metabolism, CYP3A4
-Active metabolite (T3)
 -highly PPB
-Excreted unchanged

Cytomel- T3 Hypothyroid Crisis

Neurology
All CNS Drugs:

Name Class MOA Side effects Dru What it helps

g
Inte
ract
ions

•Norepinephrine Catecholam
ines •Stimulate sympathetic nervous
(alpha- more alpha system
specific+beta)
•Receptor specificity or not!
•Epinephrine
(alpha+beta)
•Dobutamine (beta1)
•Dopamine (beta1)
Isoproterenol (Isuprel)
(alpha1, beta1, beta2)
•Phenylephrine (alpha)
•Ventolin (beta2)- used
in asthma
•Serevent (beta 2)-
used in COPD

•Mucomyst (Increase Cholinomim Stimulate parasympathetic nervous ‘cholinergic’ effects

secretions)- Clearing etics system
•Hypotension, Bradycardia
airways of mucus
•Stimulate Acetylcholine •Increased secretions
•Bladder spasms

•Pilocarpine (Decrease Cholinomim Stimulate parasympathetic nervous •topical formulation= tearing, Glaucoma tx
intraocular pressure) etics system blurry vision, headache
•eye drops (topical •Stimulate Acetylcholine •vs systemic cholinergic effects
formulation) (e.g IV)
•Effects: dilation of trabecular
•Combination meshwork = increased aqueous ‘cholinergic’ effects
treatment with humour outflow = decreased ocular •Hypotension, Bradycardia
NSAIDs- decreases pressure
inflammation in the •Increased secretions
tissue! •Bladder spasms

Nicotine (1 cigarette = •Sexual arousal •Highly addictive

10 mg of nicotine ) •Cholinomi
metic & •Decreased appetite •Crosses BBB
Adrenergic/ •Vasoconstriction/HR •Nicotine withdrawal-
Catecholam headaches, irritability, difficulty
ine •Muscle contraction
concentrating
(indirect) •Decreased perception of pain
•Decreased anxiety (Dopamine
release)
-Increased Glucose
 •High receptor affinity

•Bioavailability of nicotine when it is

inhaled is extremely high

Bupropion (Zyban, Dopamine •Nicotine via other delivery routes seizures, insomnia, headache, Nicotine
Wellbutrin) & VS changes Replacement
•Decreased bioavailability Therapy
Norepineph
rine •Decreased toxic substances other
reuptake than nicotine
inhibitor •E.g. Patch
increased dopamine &
norepinephrine

•Ephedrine (anti- ‘Indirect’

Adrenergic •Enhance release of catecholamines
secretions)
Agonists •often with release of Dopamine
•Sudafed (treats head (catecholamine precursor & CNS
cold and sinus) neurotransmitter)

Amphetamines ‘Indirect’ Drug of

Adrenergic •Enhance release of catecholamines
abuse/Performa
Agonists •often with release of Dopamine nce enhancing
(catecholamine precursor & CNS drugs/Parkinson
neurotransmitter) s
•Effects: adrenergic disease/ADHD/
Narcolepsy/Obe
•Vasoconstriction sity/Depression
•Wakefulness/focus
•Elation
•Decreased appetite

Amphetamines ‘Indirect’ weight loss, tachycardia, ADHD

Adrenergic •Enhance release of catecholamines insomnia
Methylphenidate Agonists •often with release of Dopamine
(Ritalin, Concerta) (catecholamine precursor & CNS
•Focus! neurotransmitter)
•Effects: adrenergic
 •Vasoconstriction
•Wakefulness/focus
•Elation
•Decreased appetite

Amphetamines •Addictive street

drug
Methamphetamine
(Crystal meth)-200x •Performance
higher potency (sports)
enhancing
•PO, intranasal,
substance
inhalation, injection
•Highly addictive
•Rave drug
•High = 6-8 hrs
Galantamine/ Acetylcholin Dementia
esterase •inhibition of Cholinesterase
Rivastigmine
inhibitors enzyme = decreased
•Crosses BBB neurotransmitter re-uptake
AKA
within the synapse
cholinester
ase =Increased Ach presence in
 blockers
CNS synapse

Neostigmine Acetylcholin
esterase •inhibition of Cholinesterase •For low muscle
-no BBB cross inhibitors enzyme = decreased tone!
neurotransmitter re-uptake
AKA
within the synapse
cholinester
ase =Increased Ach presence in
blockers CNS synapse

-high affinity for the somatic

nervous system Ach synapses

•Vecuronium Nicotinic
Antagonists •Block Acetylcholine binding at •Constant monitoring •Patient who
•Rocuronium nicotinic receptors of vital signs- will need needs to be
•Pancuronium to receive analgesia! paralyzed-
(SNS, PNS, and skeletal
muscle junctions) complex surgery,
Neuromuscular severe trauma
blockade -no BBB penetration accident-
•Succinylcholine (short diaphragm and
t1/2)-For patients who intercostals will
need to be intubated!
not move- anyone
•Botox (Intradermal receiving these
injection; superficial needs a ventilator!
paralysis)

Nicotinic Muscle relaxant (all muscles!!!) Adjunct to

Rocuronium Antagonist General
Onset: 1-3 min; duration Anesthesia
15-60 min
Ideal for rapid
•IV, liver metabolism & intubation &
excretion mechanical
ventilation

Poison: Curare Nicotinic •Specificity: highest to Somatic

(various South American Antagonist NS
toxic plant extracts) (anticholine
 rgic) •Mortality: respiratory muscle
paralysis

-am Benzodiaze Seizures & Status

pines Increase GABA epilepticus Tx
‘calm the brain’

Benzodiazepines work by
binding to the GABAa
neurotransmitter- opening the
chloride channel- causing a
calming effect

Diazepam (Valium) Benzodiaze Seizures & Status

pines Increase GABA epilepticus Tx
•Rapid absorption, IV
route ‘calm the brain’
•Tx of status epilepticus
Clonazepam (Klonopin)

*1st line, fast acting: Benzodiaze Anxiety, Panic Tx

pines
Midazolam (Versed)- IV,
IV infusion=longer-term,
Lorazepam (Ativan)-
sublingual
administration
•BOTH usually short
term

•long acting: Benzodiaze Anxiety, Panic Tx

pines
Diazepam (Valium),
Clonazepam (Klonopin)

Benzodiaze Benzodiazepine
Flunitrazepam pines Abuse
(Rohypnol)= roofy
•10x potency of Valium
•Intermediate acting
benzo
•Onset 15 min
•Peak 2 hrs
•Duration 4-6 hrs

Alprazolam (Xanax)

Benzodiaze Euthanasia
Benzodiazepine IV + pine and
Propofol- anesthesia Anesthesia
medication + and
Rocuronium-
neuromuscular blockade Nicotinic
Antagonist
(Neuromus
cular
Blockade)

-barbital Barbiturate Seizures & Status

s Increase GABA epilepticus Tx
‘calm the brain’

Phenobarbital; Barbiturate Seizures & Status

s Increase GABA Higher addiction risk More Drug-Drug epilepticus Tx
Pentobarbital
than Benzodiazepines interactions than
•Longer acting! ‘calm the brain’
Benzodiazepines

Barbiturate Assisted Suicide

Secobarbital s Increase GABA
•9 g PO ‘calm the brain’

Phenytoin (Dilantin); Anticonvuls Seizures & Status

ants Decrease neuronal activity => epilepticus Tx
Carbamazepine delay depolarization;+ Increase
(Tegretol), Valproic Acid GABA
(Valproate)
Gabapentin (Neurontin) Anticonvuls •increases GABA = calming •Can cause Addiction Chronic pain tx
ants
•excreted unchanged •Can cause Sedation

Antipsychot Psychosis
ics AKA Block Limbic system D2 •D2 antagonism in
neuroleptic dopamine receptors basal ganglia =>
s Extrapyramidal side
•Limbic system- main control of
effects:
mood, behavior, emotion
•Tardive dyskinesia
•degree of antagonism =
(strange tongue
success with therapy
movement),
•degree of specificity = fewer Parkinsonism (rigidity),
other effects tremors, restlessness,
•NOT addictive dystonias (muscle
spasm)
•Wide TI
•Stop/reassess tx
•High PPB

Antipsychot Psychosis
‘Typical’/Original drugs: ics AKA •associated
neuroleptic 5HT/serotonin
Chlorpromazine
s blockade;
Haloperidol (Haldol) anticholinergic;
sedation!
Onset of action:
•Anticholinergic side
•days to improvement of effects: urinary
hallucinations/delusions retention, dry mouth,
•6-8 weeks to overall sexual dysfunction
improvement •ALERT: Neuroleptic
•If change of therapy, Malignant Syndrome
slow toxic reaction:
withdrawal/‘weaning’ hyperthermia, unstable
protocols: risk of BP, diaphoresis,
Delirium tremens- rapid incontinence
onset of confusion: Physical Dependance
symptoms= irritability,
insomnia, anxiety, •The body adapts to
tremors, N&V, seizures, the presence of
hallucinations exogenous substance
 •Creates tolerance
(defined as requiring
higher doses to yield
the same effect, not
always seen for all
effects)

Antipsychot Serotonin + alpha Psychosis with

‘Atypical’ drugs: ics AKA negative
adrenergic blockade,
•Olanzapine (Zyprexa)- neuroleptic anticholinergic symptomologies –
commonly prescribed; s example-
•movement disorder
Quetiapine (Seroquel); depression
effects present
Clozapine (Clozaril)
•minimal sedation
Risperidone (Risperdal)
•depot injections
-Drug injected into the
dermis- slowly released
and slowly absorbed by
the body
-excellent for long term
therapy
-for patients who may
not remember to take
medication

•Decreases Na cellular influx = •serum monitoring !!! •interactions!!! Adjunct treatment

Lithium (Lithonate) with
‘stabilizing’ mood •preg. category D- Antipsychotics for
•low dose tx plan
=decreased impulsivity & Benefit of the drug will suicide risk
•slow onset of action (1- decreased mood swings have to out way the
3 weeks) risk to the fetus reduction

Levodopa- synthetic increase Dopamine, agonise Parkinson’s

dopamine. Rotigotine receptors Disease Tx
(Neupro)- dopamine
agonist.

Fluoxetine (Prozac), Antidepress increase Serotonin Serotonin Syndrome- 1st line*

Sertraline (Zoloft), ants too much serotonin in Depression
Paroxetine (Paxil); SSRIs the body
Citalopram (Celexa) (selective
serotonin •Symptoms occur
reuptake within minutes to
inhibitors) hours, and may
include:

•Agitation,
hallucinations

•Tachycardia, BP
changes

•N&V, diarrhea

Mirtazapine (Remeron), Antidepress increase Serotonin & Serotonin Syndrome- Depression

Bupropion (Wellbutrin) ants Norepinephrine too much serotonin in
SNRIs the body
(Serotonin
& •Symptoms occur
Norepineph within minutes to
rine hours, and may
reuptake include:
inhibitors) •Agitation,
hallucinations

•Tachycardia, BP
changes

•N&V, diarrhea

Ketamine General Causes

Anesthesia Acts on many receptors & Conscious
*part of decreases CNS excitation: Sedation
•IV
general •Decreased Glutamate (NMDA
•fast onset of action anesthetic blockade)
drug class, •Ca channel blockade
•T1/2=2-3 hrs although it
causes •Central analgesia (opioid
•Crosses BBB receptors)
conscious
sedation. • DOES NOT affect GABA
Street Drug AKA special
K, cat valium Effects:
•Sensory blockade
•short acting
•Amnesia
•Date rape drug
•Altered respirations & VS
•High sedation, •Analgesia
amnesia, resp.
•In therapeutic doses, patient
depression
appears lightly asleep

Isoflurane, Halothane, General Causes

Anesthesia Decreases sensory input: Unconsciousness
Nitrous Oxide
(inhalation) -laughing •Antagonizes NMDA-
gas decreases glutamate!
•Crosses BBB
•increases GABA

•increases endogenous opioids

secretion

•modulates and decreases

dopamine

Propofol (Diprivan) (IV) - General •No analgesia!!! Causes

Anesthesia increases GABA Unconsciousness
most commonly used •Respiratory
•Sedative hypnotic Decreases sensory input: depression
•Hypotension
•Crosses BBB
•Antagonizes NMDA- Clients who have an
•Onset: 15-30 seconds decreases glutamate! allergy to eggs or soy
•lipophilic, IV continuous products may have an
infusion, short t1/2 3 •increases GABA allergic reaction to the
min; liver metabolism; Propofol emulsion,
renal excretion •increases endogenous opioids which contains these
secretion products.
 •modulates and decreases
dopamine

Prilocaine Local Hypotension Causes

Anesthesia Na influx blockade => no numbness
-duration of action= 1-2 Sodium cellular depolarization Respiratory depression
hrs ‘blockers’ Urinary retention
Lidocaine -shorter (blocked area
duration of action dependent- commonly
seen in lumbar)
-Arrhythmia treatment
Bupivacaine •Drug dosage higher
for epidural route vs
-longer duration of
spinal route
action
Ropivacaine •Onset of drug action:
Epidural 20-30 minutes
-Higher affinity for
sensory nerve blockade
as opposed to motor
blockade
-great for labor
-no BBB unless
administered centrally!
•Onset: <2 min
•Routes: SC nerve
block- Injected near the
nerve, or inferior to the
root, epidural, spinal

•Increased vasoconstriction => Adjunct Drug to

Epinephrine •Routes: Local Anesthesia
increased localization
SC injection

•Mixed in to provide additional Adjunct Drug to

Opioids •Routes: SC, Local Anesthesia
pain relief
Epidural, Spinal
 Local Cocaine taken
Cocaine aka: blow, Anesthesia •Epinephrine re-uptake with alcohol- both
snow, nose candy, coke Sodium inhibitor !
metabolized in the
‘blockers’ •The only local anesthetic liver=
•crosses BBB, affects
enhancing vasoconstriction cocaethylene-
permeability of the BBB;
various routes of •Rarely used (ENT surgical Causes inhibition
administration procedures to decrease of cocaine
(insufflation most hemorrhaging) metabolism
common for immediate
effect); rapid onset of •Increases: epinephrine, -Cytotoxic to the
action, t1/2= 1 hr dopamine, serotonin
liver, and other
organs when
distributed

Potency of alcohol
and cocaine
becomes about
3.5x higher when
both are taken
together

Ecstasy / MDMA/ MDA Amphetami •Increases: epinephrine, •Long term: sleep

Aka: molly, clarity, ne-type + dopamine, serotonin problems, anxiety,
essence, hug, love drug hallucinoge depression,
nic impulsiveness,
•Rave drug substance anorexia, Negative
•Quick onset neuroplasticity

•Active metabolite =
extra long duration of
action (12-20 hrs)
-PO route most common
-Also comes as a
sublingual tablet in
blotting papers

Excitatory & inhibitory effects:

Alcohol (ETOH) •Often combined with
•Increased Ach, Serotonin, drugs =
•Absorption via stomach
GABA DANGEROUS!
•Crosses BBB
•Phase of stimulation followed Metadoxine -given in
•Uses vitamin B during by sedation treatment of ETOH
metabolism- Vitamin B overdose -increases
is an energy vitamin for alcohol metabolism!
our cells – preserves
•Liver toxicity/cirrhosis,
cellular function
neurotoxic
•Displays zero order
•Withdrawal syndrome
kinetics
with chronic misuse:
Delirium Tremens

ETOH overdose:
Symptomatic support,
benzodiazepines, high
dose IV vitamins

Quaaludes Sedative
hypnotics/h •Increased: serotonin &
(Methaqualone)
allucinogen dopamine
s
•NMDA (Glutamate) receptor
antagonist =>
•hallucinations, altered
perceptions/thoughts
•sedation & amnesia with
some drugs

Psilocybin (mushrooms) Sedative

hypnotics/h •Increased: serotonin &
AKA shrooms, magic
allucinogen dopamine
mushrooms, purple
passion s
•NMDA (Glutamate) receptor
Active ingredients: antagonist =>
Psilocin & Psilocybin
•hallucinations, altered
•Route: PO, tea perceptions/thoughts
•sedation & amnesia with
some drugs

Dimethyltryptamine Sedative
hypnotics/h •Increased: serotonin &
(DMT) AKA Aya
allucinogen dopamine
(Ayahuasca), dimitri,
business trip, fantasia s •NMDA (Glutamate) receptor
antagonist =>
•Route: tea; PO,
smoked, snorted, IV •hallucinations, altered
perceptions/thoughts
•sedation & amnesia with
some drugs

Phencyclidine (PCP) Sedative

hypnotics/h •Increased: serotonin &
AKA love boat, angel
allucinogen dopamine
dust
s
•Relative of Ketamine •NMDA (Glutamate) receptor
antagonist =>
•Excitation phase =>
sedation phase •hallucinations, altered
perceptions/thoughts
•Dosage dependent
•sedation & amnesia with
some drugs

Cannabinoi Short term effects: Interaction btw

•Drug: Cannabis (plant = ds Receptors:
THC & CBD: high
Marijuana) AKA dope, THC agonises CB1 and CB2 •30 min onset CBD reduces
pot, weed, grass, joint,
•CB1 receptors are found in •Altered mood THC effects (e.g.
420, ganga, texas tea
both the central and peripheral decreases
•Impaired memory anxiety-inducing
Routes: smoked, PO, nervous systems
dabbing- highly •Relaxation effects of THC)
•majority in hippocampus &
concentrated •Un-inhibition of
amygdala- amnesia
cannabinoid product behavior
(THC resin) CBD modulates CB1 & 2 +
others- Increased risk of •HR changes
 tolerance
•Smoking - most rapid •Psychosis (up to 2%
absorption (lungs to •antagonizes adrenergics; of users)
brain) increases serotonin & Long term effects:
dopamine & anandamide- what
•peak 3-10 minutes
makes us have amnesia, found •Decreased brain
•oral administration: in amygdala synapses
"edibles”
Overall effects: •Poor memory
•Slowest &
•increased appetite, decreased •Poor learning
unpredictable
pain, alterations in emotional •IQ decline with use
•lipophilic – high volume and cognitive processes
•Hallucinations
of distribution •Increased cannabinoid
receptor stimulation = loss of •Paranoia
•re-release from fatty
tissues back into the focus, memory loss
•Psychosis (upto 2% of
bloodstream = •+ Increased dopamine users)
prolonging half-life overtime- Increased risk of
addiction •Adolescence = 40%
•Metabolism: liver, increased risk
CYP450 •Psychosis risk with exposure
Withdrawal tx:
•Elimination: feces CBT (Cognitive
>65% , urine = 20% Behavioral Therapy)
•Half life: frequency of Adjunct therapy
use dependent depending on
•Studies show THC 1.3 symptoms:
days post-1x use; •Antidepressants
frequent user for 5-13
days •Antianxiety
•Gender: males have •Eg. Buspirone-
faster clearance rates anxiolytic
THC resin
Serotonin 5-HT1A
-extracted from Agonist
Marijuana. AKA shatter,
honey oil, wax, budder -benefit = doesn’t
•Highly concentrated cause sedation
THC
-adjunct or primary
•Potent treatment of
•Hallucinations
depression
•Volatile VS changes
Ex. High BP,
hyperthermia
Hashish
AKA hash, brownies,
herb, skunk, cheeba

•Cannabis plant product

•THC content varies

NUTRITION DRUGS
Name Class MOA Side effects Drug What it helps
Interac
tions

Lactaid Lactase enzyme medication Lactose Intolerance

(not in infants)

Glybera Gene A harmless viral vector delivers an Lipoprotein lipase

IM injection Therapy intact copy of the human lipoprotein deficiency (LPLD)
Drug lipase (LPL) gene

Ferrous sulfate- Iron GI pains, stomach cramps, Iron Deficiency

PO/IV/IM Dosage in elemental (available) iron
supplement constipation (decreased
Ferrous fumarate; : Ferrous •Bioavailability = 90% peristalsis), drug-drug-food
Ferrous gluconate salts interactions (calcium will
•Patient-based amount
(non-heme iron) recommendations (e.g. peds vs decrease iron absorption)
adults)

•Ideally take on empty stomach

Iron •Iron deficiency replacement: Iron Deficiency

Iron Dextran IV or
supplement calculate based on lean body weight
IM administration-
& Hgb
avoids GI upsets!
•Hemorrhage replacement: Iron mg =
 mL (blood loss) x Hct

Iron •New iron, better absorption & lower Iron Deficiency

Monoferric
supplement allergies, lower risk of free iron OD
(Monofer)

IV or IM
administration-
avoids GI upsets!

Iron Poisoning
Deferoxamine ‘chelator’; ‘chelation therapy’
(Desferal)
•chelates (binds) iron to form non-
T ½ = 6 hrs reactive complexes
•Highest affinity for ferritin &
IV administration
hemosiderin-bound iron
highest efficacy
•Low affinity for transferrin-bound iron

Vitamin D can be overdosed Vitamin D Deficiency

Calcitriol Vitamin D Active vitamin D3 (lipid soluble) S&S: fatigue
(Calcijex) Medications (also a symptom of a vitamin
•If vit D deficiency; at risk d/t
GI/liver/renal dysfunction D deficiency), GI pain, N&V,
PO
renal changes

Calcium Calcium Deficiency

Calcium
gluconate (IV or Supplement
PO), Ca acetate, s
Ca citrate, Ca
carbonate
(TUMS)- also an
antacid

GI reflux (take 30 min pre- Osteoporosis

Alendronate Biphosphon Suppress osteoclast activity = food, sit upright post dose)
(Fosamax); ates decrease rate of bone resorption.
Risedronate
(Actonel) Monitoring: bone scan annually-
(Note: people can be over-xrayed;
too much radiation)
 Ensure Plus: 1 adult serving= 237 mL
Ensure Plus; Polymeric Calories to meet BMR
Pediasure Caloric •High Calorie (350) = 10 cal/lb
(Pediatric) supplement Higher requirement:
•High fat (11 g)
s illness, malnutrition,
•High protein (13 g) malabsorption
•Carbohydrates (main immediate
energy source)
•Vitamins
•Minerals

Orlistat (Xenical) s/e: decreased lipophilic

Lipase •gastric & pancreatic lipase inhibition Obesity
medications/vitamins
inhibitors => no hydrolysis of fats => no
absorption; pregnancy
absorption; effective up to 30% of
category X; fecal fat & fecal
ingested fat
leakage (Patient may
•Overall decreased fat/triglyceride experience fecal
absorption in the intestine incontinence); GI bloating &
flatus

CNS effects -headache,

Contrave Anorexiants Bupropion (high dopamine, high Obesity
dizziness, insomnia, N & V,
(combination: - new drug norepinephrine= decrease fatigue, and seizures
Bupropion + class decrease appetite)
(Antidepres
Naltrexone) sant Pregnancy Category X -NOT
combined + Naltrexone (same binding sites as recommended for long term
with an Naloxone -longer t1/2 -PO; most use (addictive substance)
opioid known for treatment in addiction=
antagonist) decreases cravings= decreased -massive weight gain may
appetite; interrupts the natural occur once off drug
stimulation via endorphin binding)
-Weaning protocols

INFECTION DRUGS
Name Class MOA Side effects Drug What it helps
 Interactions

Xolair Monoclonal Decreasing IgE is the Allergies

(Omazilumab Antibodies goal.
)
Biologic
SC
Q 2 weeks

Human Blood To create an osmotic Allergic reactions possible though Low plasma volume
Serum product gradient that draws fluid uncommon
Albumin Collioid from the interstitial space Peripheral edema Hypovolemic shock
(Albuminar, into the vasculature; Pulmonary congestion Hypoproteinemia
Alburex, increased intravascular Clotting difficulties as dilution of
Plasbumin) volume, increases blood blood increases
IV pressure Circulatory overload if too much
fluid drawn into vasculature
Can exacerbate heart failure Renal
failure can promote fluid overload
ONCOLOGY DRUGS
Name Class MOA Side effects Drug Interactions What it helps

Nitrogen Alkylating Agents Alter DNA (cell cycle non-

mustard (cell cycle non-specific) specific) Only a few One of the earliest
-based on They work by reacting with alkylating drugs classes of drugs used to
‘mustard the proteins that bond are capable of treat cancer
causing significant
gas’, WWI together to form the very •Chemotherapy of
drug interactions.
chemical delicate double helix Hodgkin and non-
Avoid
agent structure of a DNA Hodgkin lymphoma
administering with
Busulfan molecule, adding an alkyl any other drug •Acute and chronic
Cyclophosph group to some or all of capable of lymphocytic and
amide them. This prevents the causing similar myelogenous leukemias
(Procytox) proteins from lining up as toxicities •Multiple myeloma
•Activated via they should, causing •Ovarian cancer, breast
hepatic CYP breakage of the DNA cancer
450 enzymes strands and eventual death
– causes of the cancer cell. It is •Neuroblastoma,
retinoblastoma
bladder essentially a mutation that
toxicity. takes away the cancer cell’s •Sarcoma
ability to multiply.

Vincristine Plant-derived Antineoplastic Mitotic Inhibitors (vinca •GI – •Acute lymphocytic

-Vinca Agents (cell cycle specific) alkaloids and taxanes) act nausea, leukemia
Alkaloid Vinca alkaloids – derived from during the M phase to vomiting,
Inhibits periwinkle prevent cell division so they •Hodgkin and non-
anorexia, Hodgkin lymphomas
spindle •Prevent formation of are CELL CYCLE stomatitis,
formation microtubules (necessary for cell SPECIFIC; constipation •Lymphosarcoma
during division) , abdominal •Malignant glioma
mitosis, M pain,
Vincristine is toxic to peripheral hepatotoxici •Neuroblastoma
phase (cell nerves and vinblastine creates ty •Rhabdomyosarcoma
cycle significant bone marrow
specific) suppression; they disrupt the •Skin – •Soft-tissue sarcoma
rash,
•Binds assembly of microtubules •Wilm’s tumour
alopecia
tubulin, (filaments that move (nephroblastoma)
preventing chromosomes during cell •Myelosupp
construction division), stopping cell division at ression •colorectal, lung cancer
of metaphase.
microtubules,
spindles Taxoids – derived from Pacific
yew tree
•Cell cannot
complete •Inhibit mitosis
mitosis •Act during late G2 and M phases;
stabilize microtubule bundles and
inhibit mitosis; can cause heart
arrhythmias and allergic reactions
Topoisomerase inhibitors
•Topoisomerase normally repairs
DNA damage
•Topoisomerase Inhibitors:
(etoposide and topotecan) are
nuclear enzymes that alter the
shape of supercoiled DNA. The
double helix becomes too tangled
to permit DNA replication, RNA
synthesis of DNA repair.
Topoisomerase II Inhibitors

•Etoposide (non small cell and

small cell lung cancer) and
Teniposide are derivatives of
epipodophyllotoxin.

•Exert their cytotoxic effects by

inhibiting the enzyme
topoisomerase II, which causes
breaks in DNA strands, not
allowing it to coil.

•Believed to kill cancer cells in the

late S phase and the G2 phase of
the cell cycle.

•Also treat histiocytic lymphoma

and testicular cancer.
5FU Antimetabolites Interfere with cellular •Leucovorin (reduced
MTX (cell cycle specific) Anti-cancer and
processes to damage DNA folate) used to counter
folic acid -like antimetabolite antibiotics immunosuppressive actions
formation, S phase (during effects of methotrexate
Methotrexate which DNA synthesis is (toxicities) •Osteosarcoma
-Folic acid analogue •These drugs can falsely
most active.)
-inhibits dihydrofolate substitute for purines, •Acute lymphocytic,
reductase that pyrimidines or folic acid OR (cell cycle specific) lymphoblastic leukemias
converts dihydrofolic inhibit critical enzymes •Lymphosarcoma in
acid to tetrahydrofolic involved in the synthesis or Molecules with similar
children
acid which activates function of these compounds. structure to nutrients
folic acid required for required for DNA synthesis, •Advanced-stage non-
the biosynthesis of metabolic pathways Hodgkin lymphoma
DNA, RNA and Folic acid analogues
•Are structural analogs of •Inoperable head, neck, and
proteins; thymidylate •Folic acid necessary for important natural pelvic cancers
is suppressed and DNA synthesis metabolites and can disrupt
cells are unable to •Breast cancer, lung
Purine analogues critical metabolic processes
make DNA cancers
•Some inhibit enzymes that
-Inhibits folic acid •Similar to adenine and synthesize essential cellular •Combination therapy with
reductase enzyme, guanine components surgery to maintain induced
lack of folate •Others incorporate into remission
-purines like adenine,
interferes with DNA DNA and disrupt replication
guanine and hypoxanthine •immunosuppressant
synthesis and repair and function
are bases for the
-Most effective in •Most are S PHASE
biosynthesis of nucleic acids
cells undergoing SPECIFIC but some can
rapid mitosis Pyrimidine analogues act on other phases of the
•Drug must be Similar to thymidine and cell cycle EXCEPT G0
present for an cytosine
extended time -inhibit biosynthesis of
pyrimidines, inhibit
biosynthesis of DNA and
RNA and can disrupt nucleic
acid function (cytosine and
tyrosine)
Bleomycin Antitumor Antibiotics DNA and RNA distort (cell Bone marrow
Doxorubicin (Adriamycin) (cell cycle non-specific) cycle non-specific) – limited use (very
suppression toxic)
Route – IV or direct instillation only •Identified in substances Cardiotoxic •acute
isolated from myelogenous
microorganisms Extravasation leukemia, testicular
damage carcinoma
Mechanism of action similar
to alkylating agents •Neuroblastoma
•Forms intercalated •Solid tumors of the
complexes between DNA bone, bladder,
 base pairs inhibiting DNA breast, ovary, GI
synthesis tract, lung, and
thyroid
•Inhibits activity of type II
topoisomerase •Used in
combination
therapy with
surgery, radiation
and other
antineoplastics

Tamoxifen (Nolvaldex) SERMs
(selective estrogen receptor
modifiers)
•Antagonizes estrogen receptor in
breast, agonist in other tissues (ie
bone)
•Blocking estrogen receptor in breast
reduces tumour growth
•Prophylaxis of breast cancer for
high-risk patients
•Adjunctive therapy following a
mastectomy to decrease potential for
cancer in the contralateral breast
Hormones and Hormone Bind to receptor sites that
Antagonists promote growth (cell cycle Non-cytotoxic,
(cell cycle non-specific) non-specific) typically palliative,
therapy limited to
SERMs (selective estrogen
breast or prostate
receptor modifiers) cancers
•Tissue specific agonists /
antagonists of estrogen
receptors
•Blocking estrogen receptor
at breast can limit tumour
growth
Aromatase inhibitors
•Prevent formation of
estradiol (another form of
estrogen) from androgens,
only effective post-
menopause
GnRH (gonadotropin
releasing
hormone)analogues
•Used for prostate cancer
•Initially increases
production of endogenous
testosterone, but negative
feedback mechanism stops
endogenous production

Androgen receptor blockers

 •reduce androgen
dependent stimulation of
prostate tumours

Corticosteroids
•Used for lymphomas and
leukemias

Tamoxifen, Toemifene and SERMs (selective estrogen
Fulvestrant receptor modifiers) •Block estrogen receptors
•A prodrug that is converted to active and only work against
metabolites cells that are estrogen
receptor positive
•Benefits derive from
depriving tumor cells of
the growth promoting
influence of estrogen
•Blocks estrogen
receptors in some tissues
(breast cancer benefit to
prevent growth and
proliferation) and activates
them in others (increased
bone mineral density,
reduction of LDL,
elevation of HDL)
Hot flashes, fluid •Gold standard for
retention, NV, endocrine treatment
menstrual of breast cancer
irregularities, •Used to treat
established disease
hypercalcemia, and for primary
endometrial cancer prevention of
and blood clots women at high risk
•Continuing
Tamoxifen for 10
years can almost
halve breast cancer
mortality in the
second decade
after diagnosis.
•Reduces the
incidence of breast
cancer in high risk
women by 44%
taking the drug for 4
years

Aromatase
Anastrozole Trastuzumab Inhibitors •Block estrogen from •Increase the risk of •Treat estrogen
•monoclonal antibody approved for androgenic precursors but fractures and receptor positive
HER-2 metastatic cancer and not from ovaries associated with breast cancer in
adjuvant therapy of HER-2 positive moderate to severe post-menopausal
breast cancer and HER-2 metastatic •May cause a myalgias women
gastric cancer. Adverse effects: compensatory rise in •Anastrozole is well
cardiotoxicity, manifesting often as estradiol in tolerated but most
congestive heart failure; combining premenopausal women common adverse
with paclitaxel can result in cardiac •Drugs work by depriving effects are
damage. Concurrent use with breast cancer cells of musculoskeletal
doxorubicin and other anthracyclines estrogen. pain (over 50%),
should be avoided. headache, and
menopausal
Does not cause bone marrow symptoms. N&V
suppression or alopecia, Diarrhea, dyspnea,
peripheral edema
Ado-Trastuzumab Emtansine and hypertension
•High dose Vitamin
Pertuzumab C and D may help
with myalgia and
Denosumab and Bisphosphonates bone density;
used to preserve bone integrity, increases the risk of
decrease hypercalcemia and osteoporosis and
fractures; decrease osteoclast related fracture.
activity, block tumor adhesion to
bone

Interferon alfa-2b: enhance host

immune responses and direct Biologic Response Interferons Agents that
antiproliferative effects on cancer Modifiers stimulate the body's
•Suppress cell division in
cells in melanoma, CML (Chronic certain cancers immune system to
myelogenous leukemia), AID related (Immunostimulants) kill tumor cells.
Kaposi sarcoma Adverse effects: •Activate macrophages
can cause flu like syndrome, and T cytotoxic cells
cardiotoxicity and bone marrow
suppression, depression BCG Interleukins
vaccine: infectious live attenuated •IL-2 activates T cytotoxic
mycobacterium bovis approved for cells and B cells (to
carcinoma of the bladder. plasma cells to
antibodies)

Hematopoietic growth
factors
•Promote formation of
blood cells to reduce
complications from
myelosuppression

•Bind specific antigens on

CD20 Directed Antibodies used to Monoclonal Antibodies Specially
cancer cells
treat B cell non Hodgkin's lymphoma engineered
 •Act as a target for
and B cell CLL (Chronic Lymphocytic (MABs) molecules that
complement, resulting in
Leukemia) attack cancer
(cell cycle non-specific) destruction of cancer cells antigens
Rituximab: causes severe infusion
related hypersensitivity reactions, Antibodies utilized
SJS (Stevens-Johnson syndrome), for various
reactivation of Hep B outcomes, e.g.:
Mark cancer cells to
Cetuximab
enhance & direct
Efficacy: metastatic colon cancer immune response

Decrease vascularization of tumor

areas

Brentuximab Vedotin: antibody drug

conjugate; binds with CD30 on the
surface of some cancer cells:
Hodgkins’ lymphoma; manageable
side effects

Bevacizumab: used in patients with

metastatic colorectal cancer.

Adverse effects: GI perforation,

hemorrhage, and thromboembolism;
Binds with VEGF (Vascular
endothelial growth factor)

High dose Glucocorticoids Suppression of mitosis; To benefit patients

suppression of N&V, with cancer, doses
reduction of cerebral must be high; treat
edema, reduction of pain cancers arising
and suppression of from lymphoid
hypercalcemia tissue CLL (Chronic
Lymphocytic
Leukemia),
Hodgkin's disease,
NHL (Non-
Hodgkin’s
lymphoma)

Angiogenesis Inhibitors Suppress formation of Liver cancer

new blood vessels and
 deprive solid tumors of
expanding their blood
supply for continued
growth; don’t kill cancer
cells.

Finasteride 5α-reductase inhibitor Role of 5 alpha-reductase Recently shown to

= enzyme that converts prevent the
testosterone to DHT development of
(dihydrotestosterone= prostate cancer in
more potent form of men without BPH
testosterone)