Drug Name
Drug Class Mechanism Distinguishing Chem Characteristics (Unique or "weird" features) Pharmacological characteristics Side Effects Special side effects Use [mnemonic] (put in brackets)
Bethanechol
-Muscarinic Cholinergic agonist - -CH3(down nicotinic) and NH2 (down AChE) -oral or subQ - -treat depressed smooth muscle activity (ileus, megacolon)
carbachol
-muscarinic cholinergic agonist
-Stim M3 receptor on ciliary body & iris improving uveoscleral outflow
-NH2 grp. Poor substrate for AChE
-oral or subQ
-
-miotic. open or closed angle glaucoma.
methacholine
-muscarinic cholinergic agonist - -CH3 decreases nicotinic affinity -oral or subQ - -often used to suppress tachycardia
muscarine
-muscarinic cholinergic agonist - -alkaloid -oral or subQ - -
pilocarpine
-Muscarinic Cholinergic agonist
-Stim M3 receptor on ciliary body & iris improving uveoscleral outflow
-alkaloid
-topical use for eye
-sweat glands particularly sensitive
-acute closed or open angle glaucoma, increase salivary secretion
[tears, saliva on your “pillow”]
varenicline
-Nicotinic cholinergic agonist - -alkaloid - - -
ambenonium
-cometitive inhibitor of cholinesterase
-carbamoylates AChE at esteratic site
-carbamate
-4-8 DOA
-
-myasthenia gravis, neuromuscular bloackade
edrophonium
-competitive cholinesterase inhibitor
-antagonize competitive inhibitor of NMJ
-alcohol w/ quaternary ammonium group
-short DOA
-
-myasthenia gravis, ileus, arrhythmias
neostigmine
-competitive cholinesterase inhibitor
-carbamoylates AChE at esteratic site, antagonize NMJ comp. inhibitors
-carbamate
-med DOA
-
-myasthenia gravis, neuromuscular blockade, ileus
physostigmine
-competitive cholinesterast inhibitor
-carbamoylates AChE at esteratic site
-carbamate
-med DOA
-
-glaucoma
diisopropylfluorophosphate
-noncompetitive cholinesterase inhibitor
-irreversible phosphoryl AChE at esteratic site
-
-
-
-insecticide
echothiophate
-Organophosphate Derivative
-Non - Competitive AChE inhibitor
-
-
-
-
- Used to treat glucoma
carbaryl
-noncompetitive cholinesterase inhibitor
-phoshphoryl group in AChE esteratic site
-
-
-
-insecticide
malathion
-noncompetitive cholinesterase inhibitor
-phoshphoryl group in AChE esteratic site
-
-
-
-insecticide
parathion
-noncompetitive cholinesterase inhibitor
-phoshphoryl group in AChE esteratic site
-
-
-
-insecticide
tetraethylpyrophosphate
-noncompetitive cholinesterase inhibitor
-phoshphoryl group in AChE esteratic site
-
-
-
-insecticide
sarin
-noncompetitive cholinesterase inhibitor - - - -nerve gas
soman
-noncompetitive cholinesterase inhibitor - - - -nerve gas
pralidoxime
-AChE reactivator
-release phosphoryl moeity in AChE esteratic site
-2-PAM
-Must B4 AChE aging occurs
-
-supplement atropine in O-P intoxication
atropine
- muscarinic cholinergic antagonist
- antagonize O-P by competitively bind muscarinics, block M3 on iris & ciliary muscle
- tertiary amine
- doses limited due to crosss BBB, long DOA, (salivary,bronch,sweat+++), bound by melanin in iris
- no alleviation of neuromusc hyperactivity, CNS effects!
- May elicit acute glaucoma
- O-P intoxication,block paraSNA, mydriasis/cycloplegia (7-10 days)
homatropine
-muscarinic cholinergic antagonist
-block M3 on iris & ciliary muscle
-tertiary amine
-med DOA
-
-mydriasis/cycloplegia (1-3 days) EYE EXAM!
scopolamine
- Muscarinic Cholinergic antagonist
- block M3 on iris & ciliary muscle
- tertiary amine
- long DOA, quick CNS, (injection, oral, transdermal only)
- sedation/amnesisa, dry mouth
- anti-motion sickness, adjunct for pre-amnesia, mydriasis/cycloplegia (3-7 days)
methscopolamine
-Muscarinic Cholinergic antagonist - -quaternary ammonium -longer DOA - -GI diseases, can inhibit respiratory tract secretions
trihexyphenidyl
-muscarinic cholinergic antagonist - -tertiary amine -3-6hrs DOA - -anti-parkinson, excess salivation
tropicamide
-Muscarinic Cholinergic antagonist
-Block M3 on iris & ciliary muscle
-
-short DOA, only topically
-
-mydriasis and cycloplegia (1/4 day)
cyclopentolate
-muscarinic cholinergic antagonist
-block M3’s on iris & ciliary muscle
-
-med DOA
-
-
-Elicit mydriasis & cycloplegia (1 day)
ipratropium
-Muscarinic Cholinergic antagonist - -quaternary ammonium -shorter DOA, topical inhalant -tachycardia, decreased salivation -bronchodilation and min. mucociliary clearance problems
tiotropium
-Muscarinic Cholinergic antagonist - - -longer DOA, topical - -bronchodilation and min. mucociliary clearance problems
darifenacin
- M3 selective cholinergic antagonist - - -longer DOA - -
solifenacin
-M3 selective cholinergic antagonist - - -longer DOA - -
tolterodine
-M3 selective cholinergic antagonist - - - longer DOA - -
mecamylamine
- N1 non-depolarizing cholinergic competitive antagonist
- ganglionic blocker
- secondary amine (improve GI absorb)
- Med DOA 12 hours
- CNS-tremor, confusion, seizure, mania, depression
- hypertensive emergency,periph vasc disease
trimethaphan
- N1 non-depolarizing Cholinergic competitive antagonist
- ganglionic blocker
- sulfonium+
- shrot DOA, intravenous
- hypotension, brain anoxia
- surgically to reduce bleeding=controlled hypotension
succinylcholine
-N2 non-competitive depolarizing inhibitor
-agonist for Na channel and keeps it open
-
-hydrolysis from plasma ChE nor AChE!, short DOA
-K–>cardiac arrest, contraction of eye muscles
-relax muscles during surgery/vent
curare
-N2 competitive inhibitor - -quaternary nitrogens - - -
atracurium
-benzylisoquinolines
-Competitive Nicotinic N2 blocker (N2 Specific)
-Non-depolarizing – Prevent Depolarization
-Intermediate in duration
-Histamine Release (hypotension) is side effect
-
-Muscle relaxation (e.g. before surgery)
cisatracurium
-benzylisoquinolines
-N2 competitive inhibitor
-Competitive Nicotinic N2 blocker (N2 Specific)
-quaternary nitrogens
-medium DOA
-histamine release
-
mivacurium
-benzylisoquinolines
-N2 competitive inhibitor
-Competitive Nicotinic N2 blocker (N2 Specific)
-
-short DOA
-histamine release
-
pancuronium
- Ammonio Steroids
- ## Competitive Nicotinic N2 blocker-
-long DOA
-muscarinic block-vagal blockade, tachycardia
-
vecuronium
-N2 competitive inhibitor
-Competitive Nicotinic N2 blocker
-quaternary nitrogens
-med DOA
-muscarinic block-vagal blockade, tachycardia
-
albuterol
-Beta-2 agonist
-stim adenyl cyclase and cAMP–>relax bronch smooth m.
-
-short DOA
-tachycardia, muscle tremor, headache
-bronchodilate acute asthma
salmeterol
-Beta-2 agonist
-stim adenyl cyclase and cAMP–>relax bronch smooth m
-
-long DOA
-tachycardia, muscle tremor, headache
-bronchodilate
salmeterol with fluticasone
-Beta-2 agonist with corticosteroid
-stim adenyl cyclase and cAMP–>relax bronch smooth m
-
-combination necessary in maintenance therapy
-
-maintenance bronchodilation
beclomethasone
-corticosteroid
-inhibit inflam. response system thru gene expression
-
-topical inhalation
-generally none
-long term asthma reduction
budesonide
-corticosteroid
-inhibit inflam. response system thru gene expression
-
-topical inhalation
-generally none
-long term asthma reduction
fluticasone
-corticosteroid
-inhibit inflam. response system thru gene expression
-
-topical inhalation
-generally none
-long term asthma reduction
prednisone
-corticosteroid
-inhibit inflam. response system thru gene expression
-
-oral or intravenous
- glucose metab.,Cushing’s, hypert, increased infection
-asthma
triamcinolone
-corticosteroid
-inhibit inflam. response system thru gene expression
-
-topical inhalation
-generally none
-long term asthma reduction
montelukast
-leukotriene modulator
-receptor antagonist of LTD4
-
-oral
-
-long-term controller of asthma
zafirlukast
-leukotriene modulator
-receptor antagonist of LTD4
-
-oral
-
- long term controller of asthma
zileuton
-leukotriene modulator
-inhibitor of 5-lipoxygenase inhibiting synthesis of LTB/D4
-
-oral
-liver toxicity, and inhibits some CYPs
-long term controller of asthma
cromolyn
- degranulation inhibitor
- possible inhibit of Ca channels in Mast cell degranulation
- poorly soluble salt
- Topical
- well tolerated
- long term prophylactic maintenance of asthma
nedocromil
- degranulation inhibitor
- possible inhibit of Ca channels in Mast cell degranulation
- poorly soluble salt
- Topical
- well tolerated
- long term prophylactic maintenance of asthma
ipratropium
-muscarinic cholinergic antagonist - -quaternary ammonium -shorter DOA, topical inhalant -tachycardia, decreased salivation -bronchodilation and min. mucociliary clearance problems
theophylline
- Misc. Bronchodilator
- inhibit phosphodiesterase degradation of cAMP
- methylxanthine
- oral, LongDOA
- tachycardia and CNS stimulation
- long-term maintenance of asthma
Drug Name
Drug Class Mechanism Distinguishing Chem Characteristics (Unique or "weird" features) Pharmacological characteristics Side Effects Special side effects Use [mnemonic] (put in brackets)
metaraminol
Alpha-1 Selective Agonist - - - Long acting beta 1 and alpha 1 stimulant, Displaces NE - - -
methoxamine
Alpha-1 Selective Agonist (less alpha 2) - - - - - - treat hypotensive crisis
phenylephrine
Alpha-1 Selective Agonist (less alpha 2) - - Long acting - - - - Vasoconstriction, prevent shock, nasal decongestant, treat hypotensive crisis, reduce drug diffusion, reduce mucus membrane congestion, mydriasis
alpha-methyldopa
*α2 selective agonist/false transmitter
*MNE (α-methyl NE) causes potent stimulation in vasomotor area of brainstem
*converted to MNE by NE synthetic pathway (partially replaces DOPA); MNE replaces NE in vesicles but greatly reduced efficacy than NE
*
*sedation, xerostomia, anorexia, fluid retention, vivid dreams, & CNS stimulation (all diminish over time)
*dizziness, sleep disturbances, impotence, dry mouth, nasal congestion (diminish after 2 weeks), postural hypotension; chronic therapy may result in hemolytic anemia, leukopenia, hepatitis, lupus-like problems
*hypertension
clonidine
*α2 selective agonist
*stimulate both PNS & CNS α2 receptors - inhibit NE release by nerve terminal (elicit hypotension by decr. TPR, HR, CO)
*
*
*sedation, xerostomia, anorexia, fluid retention, vivid dreams, & CNS stimulation (all diminish over time)
*
*hypertension
apraclonidine
*α2 selective agonist
*stimulate both PNS & CNS α2 receptors - inhibit NE release by nerve terminal (elicit hypotension by decr. TPR, HR, CO).
*
*
*sedation, xerostomia, anorexia, fluid retention, vivid dreams, & CNS stimulation (all diminish over time)
*
*hypertension, EXTREME open angle glaucoma
guanabenz
*α2 selective agonist
*stimulate both PNS & CNS α2 receptors - inhibit NE release by nerve terminal (elicit hypotension by decr. TPR, HR, CO)
*
*
*sedation, xerostomia, anorexia, fluid retention, vivid dreams, & CNS stimulation (all diminish over time)
*
*hypertension
amphetamine
Alpha and beta adrenergic agonist - - Releasing agent (increases NE release), also releases intraneuronal NE – reverse transport - - - -
ephedrine
-
- Releasing agent, Stimulant of most adrenergic receptors, Long acting – Displaces NE
-
-
- Increase CO and arterial pressure, treat orthostatic hypotension, reduce mucus membrane congestion, stress incontinence
epinephrine
Alpha and beta adrenergic agonist - - - Binds all adrenergic receptors equally - - - Potent vasoconstrictor and cardiac stimulant, hemostasis during surgery, reduce drug diffusion, anaphylaxis
norepinephrine
-
- Binds Beta-2 a lot less than all other adrenergics
-
-
- IV infusion for shock, increase CO and cause vasoconstriction (increase BP, treat hypotensive crisis), reduce drug diffusion
dipivefrin
*Mixed alpha, beta agonist
*stim alpha 2 on ciliary body, alpha 1 on ciliary vessels
*Prodrug metabolized to Epi.
*
*
*
*Open angle glaucoma
dobutamine
Beta 1 Selective agonist - - -(Less binding to beta-2) - - - Cardiogenic shock, heart failure
isoproterenol
Beta 1 and 2 agonist - - - - - - Used for relaxation of bronchial smooth muscle, also cardiac stimulation (potent vasodilator)
albuterol
Beta 2 Selective agonist - - -(Less binding to beta-1) - - - Bronchial asthma
metaproterenol
Beta 2 Selective agonist - - -(Less binding to beta-1) - - - Bronchial asthma
terbutaline
Beta 2 Selective agonist - - -(Less binding to beta-1) - - - Bronchial asthma, relax pregnant uterus
bromocriptine
-
-
- postural hypotension and cardiac arrhythmia
-
- Anti-parkinson agent (for its CNS effects)
dopamine
-
- Binds Alpha and Beta 1 at high concentrations, Enhance NE release (displaces it)
-
-
- IV for shock, vasoconstriction, increase CO and dilate renal arteries
fenoldopam
Dopamine Agonist, DA-1 selective - - - - - - Vasodilation of renal and mesenteric vessels
doxazosin
Alpha-1 Selective antagonist - - - - - - Urinary obstruction from BPH
prazosin
-
- Oral admin
-
- Little to no tachycardia because doesn’t bind beta receptors
- Antihypertensive (mild / moderate), urinary obstruction from BPH
tamsulosin
Alpha-1 Selective antagonist - - - - - - Urinary obstruction from BPH
terazosin
Alpha-1 Selective antagonist - - - - - - Urinary obstruction from BPH
phenozybenzamine
Alpha-1 and Alpha-2 Selective antagonist
- Non-competitive – alkylates alpha receptors (~24 hrs)
- ## Can cause postural hypotension and tachycardia – due to decreased MAP
- Used to treat hypertension associated with pheochromocytoma
phentolamine
Alpha-1 and Alpha-2 Selective antagonist
- Competitive antagonist
-
- Dirty drug, binds histamine and muscarinic receptors
- Increases NE release, will cause tachycardia and increased CO
-
- Diagnostic for pheochromocytoma, also for its assoc. hypertension
labetalol
Alpha and beta antagonist - - Binds beta receptors better than alpha - - - -
atenolol
*β1 selective antagonist
*inhibit CO; class generally pure antagonist (binds but does not activate receptor)
*β1»_space;> β2; t1/2=6-9 hours; diminished ability to cross BBB
*combination with diuretics and other antihypertensive agents
*
*less prone to induce bronchial smooth muscle constriction in asthma patients; fewer CNS effects
*hypertension
betaxolol
*β1 selective antagonist
*block B1 receptors on ciliary body to reduce aq. humor production; inhibit CO; class generally pure antagonist
*β1»_space;> β2; ; t1/2=14-22 hours
*combination with diuretics and other antihypertensive agents
*
*less prone to induce bronchial smooth muscle constriction in asthma patients
*Open angle glaucoma; hypertension
metoprolol
*β1 selective antagonist
*inhibit CO; class generally pure antagonist
*β1»_space;> β2; t1/2=3-4 hours
*combination with diuretics and other antihypertensive agents
*
*ataxia, dizziness; less prone to induce bronchial smooth muscle constriction in asthma patients
*hypertension, angina pectoris; prophylaxis for MI recurrence
nadolol
*β non-selective antagonist
*inhibit CO & dilation/relaxation
*β1 = β2; t1/2=14-24 hours; diminished ability to cross BBB
*combination with diuretics and other antihypertensive agents
*may inhibit dilation of bronchioles (significant in asthma patients); may induce cardiac failure (significant in cardiac insufficiency patients); fewer CNS side effects
*
*hypertension
pindolol
*β non-selective antagonist
*inhibit CO & dilation/relaxation
*β1 = β2; t1/2=3-4 hours
*combination with diuretics and other antihypertensive agents
*may inhibit dilation of bronchioles (significant in asthma patients); may induce cardiac failure (significant in cardiac insufficiency patients)
*
*hypertension
propranolol
*β non-selective antagonist
*inhibit CO & dilation/relaxation
*β1 = β2; t1/2=3-6 hours
*
*may inhibit dilation of bronchioles (significant in asthma patients); may induce cardiac failure (significant in cardiac insufficiency patients)
*ataxia, dizziness
*hypertension, arrhythmia, angina pectoris, migraine headache; prophylaxis for MI recurrence
timolol
*B non-selective antagonist
*block B1R’s on ciliary body to reduce aq. humor production ->lower intraocular pressure;
*t1/2=4-5 hours
*topical for glaucoma
*may inhibit dilation of bronchioles (significant in asthma patients); may induce cardiac failure (significant in cardiac insufficiency patients)
*
*Open angle glaucoma, antihypertensive, angina pectoris; prophylaxis for MI recurrence
carteolol
*B non-selective antagonist
*block B1R’s on ciliary body to reduce aq. humor production
*
*topical
*
*
*Open angle glaucoma
levobunolol
*B non-selective antagonist
*block B1R’s on ciliary body to reduce aq. humor production
*
*topical
*
*
*Open angle glaucoma
metipranolol
*B non-selective antagonist
*block B1R’s on ciliary body to reduce aq. humor production
*
*topical
*
*
*Open angle glaucoma
guanethidine
*pre-junctional inhibition of NE release
*stabilizes neuronal membranes, interfering with exocytosis of NE vesicles
*transported into adrenergic neurons via Amine I transport; does not cross BBB
*orally effective
*
* chronic administration->depleting NE within synaptic vesicles; minimal adverse CNS effects; minimal effects with other biogenic amines
*hypertension – reserved for therapy of most severely elevated arterial pressures
reserpine
*pre-junctional inhibition of NE release
*depletes stores of biogenic amines (Epi, NE, DA, serotonin) in both CNS & PNS by blocking transport into storage vesicles
*long DOA; very potent
*orally effective
*
*increased GI motility (>ulcers); CNS: sedation, depression, parkinsonian symptoms
*hypertension
cocaine
*Amine I transport (NET) inhibitor
*NE levels rise in synapse -> mimic sympathetic nerve stimulation
*
*
*vasoconstriction, tachycardia, mydriasis
*
*hemostasis during surgery
DMI (desmethylimipramine)
*Amine I transport (NET) inhibitor
*NE levels rise in synapse -> mimic sympathetic nerve stimulation
*
*
*vasoconstriction, tachycardia, mydriasis
*
*
tyramine
Releasing Agent - - - Enhance NE release via Amine 1 transporter - - -
pseudoephedrine
Releasing Agent - - - - - - Reduces congestion of mucus membranes
Drug Name
Drug Class Mechanism Distinguishing Chem Characteristics (Unique or "weird" features) Pharmacological characteristics Side Effects Special side effects Use [mnemonic] (put in brackets)
Azathioprine
- General Growth Inhibitors
- ## Metabolized to 6-mercaptopurine then 6 thioguanine (blocks purine synthesis). Also incorporates into DNA
- Inactivated by xanthine oxidase
- ## Myelosuppression, nausea, vomiting
- Used for renal and other tissue transplantation, autoimmune disease, and gout
Cyclophosphamide
-General Growth Inhibitors
-Cross links DNA, kills all proliferating cells
-
-
- Myelosuppression, nausea, vomiting,
- Infertility
- Used for autoimmune diseases, bone marrow transplant
Leflunomide
*General Growth Inhibitors
- Decreases pyrimidine synthesis
-
-
- Diarrhea, modest hepatotoxicity, reduced myelosuppresion
-
- Used for Rheumatoid arthritis, some autoimmune disease
Methotrexate
*-General Growth Inhibitors
- Inhibits dihydrofolate reductase, prevents thymidide and purine synthesis
-
-
- Causes nausea, mucosal ulcers, modest hepatotoxicity, reduced myelosuppression
-
- Rheumatoid arthritis, some autoimmune disease
Mycophenolate Mofetil
*-General Growth Inhibitors
- prevents purine synthesis
-
-Prodrug of mycophenolic acid, active form
- myelosuppression, nausea, vomiting
-
- Used for solid organ transplant (cyclosporine alternative) autoimmune disease
Prednisone
*-Glucocorticoid
-Upregulates / Downregulates expression of genes assoc. with inflammation and immunosuppression (e.g. IL2 and IFN-gamma). Inhibition of annexins genes (thus phospholipase A2). Esp. affects IL-2 & IFNgamma
- No serious bone marrow toxicity
-
-
- Cushings syndrome, osteoporosis, glucose intolerance, hypertension, susceptibility to infection
- Used for solid organ transplantation (first line), stem cell transplantation, autoimmune diseases, asthma, allergic reactions, systemic inflammation
Sirolimus
*- mTOR inhibitor
- Binds FKBP12 to form complex that inhibits IL2 activation
-
- Antagonizes tacrolimus, synergistic with cyclosporine
- Myelosuppression, hyperlipidemia, hypertension, edema, hepatotoxicity
-
- Solid organ transplants, steroid resistant graft v. host disease
Cyclosporin
*- Calcineurin inhibitor
- Binds Cyclophilin to form complex that inhibits NFAT activation
-
- Often combined with other immunosuppressant agents
- Nephrotoxicity, hypertension, hyperglycemia, liver dysfunction.
- Increased cancer incidence documented
- Kidney, liver and cardiac transplants, inflammatory diseases (asthma) & autoimmune
Tacrolimus
*- Calcineurin inhibitor
- Binds FKBP12 to form complex that inhibits NFAT activation
-
- 10-100 X more potent than cyclosporine
- Nephrotoxicity, hypertension, hyperglycemia, liver dysfunction.
- Increased cancer incidence documented
- Kidney, liver and cardiac transplants, inflammatory diseases (asthma)
Anti-T cell globulin
- Antibody / Fusion Protein
- Blocks T cell surface receptors and opsonizes T cells
- Product of repeated injection of human T cells into animals
- Cytokine release syndrome (reduce w/ pretreat. With acetaminophen and antihistamine, serum sickness
- Anaphylaxis potential (with repeat use)
- Prevent maternal (Rh-) from attacking fetus
Alemtuzumab (anti CD52)
*- Antibody / Fusion Protein
- Depletes cells expressing CD52 (T and B cells, monocytes, macrophages, NK cells)
- Prolonged depletion (1 yr) of T cells and other immunecells
-
- Myelosuppresion, flu like symptoms
-
-
Basiliximab (Anti CD25)
*- Antibody / Fusion Protein
- Blocks and opsonizes alpha chain of IL-2 (CD25), found only on activated T cells
- Depletes only antigen activated T cell , reduced incidence of infection and malignancy
- Moderate effect relative to anti-T cell globulin
- Well tolerated
-
-
Rh(D) immune globulin
*- Antibody / Fusion Protein
- Binds and clears up D-antigen, prevents mother’s immune rxn
-
-
-
-
- Prevent maternal (Rh-) from attacking fetus
Belatacept
*- Antibody / Fusion Protein
- Fusion of IgG and high-affinity B7 ligand, so without this signal acting on CD28 T cells go into anergy when presented with an antigen. (Binds and clears up D-antigen, prevents mother’s immune rxn?)
-
- Comparable to calcineurin inhibitors in preventing transplant rejection
- Anemia, neutropenia, peripheral edema
- Increased risk of infection and malignancy, especially post-transplant lymphoproliferative disorder
- Use for kidney transplant
Interleukin-2
*- Cytokines
- Increases proliferation of activated T cells, increases IFN-gamma and cytotoxic killer cell activity
-
-
- Capillary leak syndrome, hypotension, reduced organ perfusion, can be fatal
-
- Used to treat metastatic melanoma, renal cell carcinoma
IFN-gamma
*- Cytokines
- Stimulates activity of cytotoxic cells
-
-
-
-
- Severe recurrent infections
BCG
*-Adjuvant
- Increases APC activity by binding pattern recognition receptors
- Live attenuated bacillus calmette-guerin
- Can’t use systemically, will cause septic shock
-
-
- Used topically for bladder cancer
Drug Name
Drug Class Mechanism Distinguishing Chem Characteristics (Unique or "weird" features) Pharmacological characteristics Side Effects Special side effects Use [mnemonic] (put in brackets)
acetazolamide
*Carbonic anhydrase inhibitor
*reduce HCO3 production to slow aq. humor production
*
*
*diuretic
*
*Open angle glaucoma
dichlorphenamide
*Carbonic anhydrase inhibitor
*reduce HCO3 production to slow aq. humor production
*
*
*diuretic
*
*Open angle glaucoma
dorzolamide
*Carbonic anhydrase inhibitor
*reduce HCO3 production to slow aq. humor production
*TOPICAL
*
*diuretic
*
*Open angle glaucoma
botulinum toxin A
*Miscellaneous
*Paresis of skeletal muscle (relaxation 3-6 wk duration) because presynaptic vesicles can’t exocytose
*Injected
*Use EMG to confirm needle placement
*diuretic
*
*extraocular muscles (squint) & blepharospasm of eyelid.
Drug Name
Drug Class Mechanism Distinguishing Chem Characteristics (Unique or "weird" features) Pharmacological characteristics Side Effects Special side effects Use [mnemonic] (put in brackets)
cetirizine (Zyrtec®)
- Second-Generation H1 Antihistamine
- ## Block histamine at H1 receptors
- ## High selectivity for H1 sites and has few anti-cholinergic side effects; Penetrates poorly into CNS, reducing sedative effects-
- allergies
[mnemonic] (put in brackets)
cyclizine (Marezine®)
- First-Generation H1 Antihistamine
- ## Block histamine at H1 receptors-
- Sedation
- Anticholinergic effects (Atropine-like effects toward muscarinic receptors, dry mouth, urinary retention, tachycardia)
- motion sickness
[mnemonic] (put in brackets)
dimenhydrinate (Dramamine®)
- First-Generation H1 antihistamine
- ## Block histamine at H1 receptors-
- Sedation
- Anticholinergic effects (Atropine-like effects toward muscarinic receptors, dry mouth, urinary retention, tachycardia)
- motion sickness
[mnemonic] (put in brackets)
diphenhydramine (Benadryl®)
- First-Generation H1 antihistamine
- ## Block histamine at H1 receptors-
- Sedation
- Anticholinergic effects (Atropine-like effects toward muscarinic receptors, dry mouth, urinary retention, tachycardia); Local anesthesia: Block sodium channels
- motion sickness
[mnemonic] (put in brackets)
fexofenadine (Allegra®)
- Second-Generation H1 Antihistamine
- ## Block histamine at H1 receptors
- ## High selectivity for H1 sites and has few anti-cholinergic side effects; Penetrates poorly into CNS, reducing sedative effects-
- Allergies
[mnemonic] (put in brackets)
loratadine (Claritin®)
- Second-Generation H1 Antihistamine
- ## Block histamine at H1 receptors
- ## High selectivity for H1 sites and has few anti-cholinergic side effects; Penetrates poorly into CNS, reducing sedative effects-
- Allergies
[mnemonic] (put in brackets)
promethazine (Phenergan®)
- First-Generation H1 Antihistamine
- ## Block histamine at H1 receptors-
- Sedation
- Anticholinergic effects (Atropine-like effects toward muscarinic receptors, dry mouth, urinary retention, tachycardia); Local anesthesia: Block sodium channels
- antiemetic
[mnemonic] (put in brackets)
adalimumab (Humira®)
- anti-TNFalpha agent
- Binds to TNFalpha, prevents it from binding to its receptor and reduces circulating levels
- Human antibody to TNFalpha
- Parenteral administration required
- increased frequency of infections (upper
respiratory, urinary)
-
-Rheumatoid arthritis, Crohn’s
[mnemonic] (put in brackets)
etanercept (Enbrel®)
- anti-TNFalpha agent
- Binds to TNFalpha, prevents it from binding to its receptor and reduces circulating levels
- Fusion protein containing the ligand binding domain of the
TNFalpha receptor and the Fc domain of human IgG. - Parenteral administration required
- increased frequency of infections (upper
respiratory, urinary)
-
-Rheumatoid arthritis, Crohn’s
[mnemonic] (put in brackets)
infliximab (Remicade®)
- anti-TNFalpha agent
- Binds to TNFalpha, prevents it from binding to its receptor and reduces circulating levels
- Humanized antibody to TNFalpha
- Parenteral administration required
- increased frequency of infections (upper
respiratory, urinary)
-
-Rheumatoid arthritis, Crohn’s
[mnemonic] (put in brackets)
anakinra (Kineret®)
- Anti-IL1 agent
- ## Competitive IL-1 receptor antagonist (IL-1Ra analog)
- Short half-life, daily injection required
Increased susceptibility to infection
- - Rheumatoid Arthritis, possibly other inflammatory diseases
[mnemonic] (put in brackets)
tofacitinib (Xeljanz®)
- Jak kinase inhibitor
- Inhibits all activity of cytokines required for adaptive immunity (eg., IL-2, IL-4, etc.) and inhibits all activities for many inflammatory cytokines (eg., IL-6)
Distinguishing Chem Characteristics (Unique or “weird” features) - oral administration; therapeutic doses chosen to produce incomplete Jak inhibition, because higher doses expected to produce potent
immunosuppression AND adverse effects. - ## Anemia, neutropenia, general myelosuppression, increased risk of infection (especially Herpes Zoster)
- RA: Currently second line therapy for those failing methotrexate
[mnemonic] (put in brackets)