Who are we?

We are GABAa receptor agonists used to treat insomnia

What are we and what do we treat?

Depakote (valproic acid), Topamax (topiramate), Tegretol (carbamazepine), Dilantin (phenytoin)

What are we and what do we treat?

Neurontin (gabapentin), Lyrica (pregabalin) and Keppra (levetiracetam)

Ca2+ channel inhibitors used to treat Seizures/Epilepsy

Neurontin (gabapentin) and Keppra (levetiracetam) can be used to treat bipolar

Who am I?

I am a benzodiazepine used to treat seizures/epilepsy

Who am I and how do I work?

I am used to treat the manic behavior of bipolar disorder

Lithobid (lithium carbonate)

Alters Na transport in nerve and muscle cells

What are we used to treat?

Tegretol (carbamazepine), Neurontin (gabapentin), Keppra (levetiracetam), Lamictal (lamotrigine)

Bipolar (mood stabilizers)

Neurontin, Keppra, and Tegretol are also used for seizures/epilepsy

Who am I?

I am an antiviral drug used to treat Parkinson's

Who am I?

I am an alpha 2 receptor agonist used as a muscle relaxant

What are we used to treat and what are our MOAs?

Zanaflex (tizanidine)

Flexeril (cyclobenzaprine)

Skelaxin (metaxalone)

Muscle Relaxants

Zanaflex= Alpha 2 receptor agonist

Flexeril and Skelaxin= unknown

Who are we?

We are used to treat HTN and we block absorption in the distal tubule

What do we treat and what is our MOA?

Lasix (furosemide), Bumex (bumetanide) and Demadex (torsemide)

HTN 

Loop diurectics

block absorption in the ascending loop of henle

What do I treat and what is my MOA?

Altace (ramipril)

Treats HTN

ACE inhibitor (drugs ending in "pril")

What do I treat and what is my MOA?

Cozaar (losartan)

Treats HTN

Angiotensin II receptor antagonist

(drugs ending in "sartan")

What do we treat and what is our MOA?

Aldactone (spironolactone), Inspra (eplerenone), Midamor (amiloride) and Dyrenium (triamterene)

Treats HTN

Aldosterone receptor antagonist (K+ sparing)

How do we work?

Nitrates used for HTN

What is our common ending?

Calcium channel blockers for HTN

We are known for causing gingival hyperplasia

The "Dipines"

Norvasc (amlodipine)

What is our common ending?

We are alpha 1 antagonists used for HTN

The "zosins"

Minipress (prazosin), Cardura (doxazosin), and Hytrin (terazosin)

What do I treat and what is my MOA?

Catapres (clonidine)

Treats HTN

Alpha 2 agonist (inverse agonist)

inhibits release of NE= vasodilation

do not take me with CNS depressants

What is our common ending?

beta 1 antagonists used to treat HTN, ischemic heart disease, angina, and CHF

olols

Toprol (metoprolol), Tenormin (atenolol), etc

What do I treat and what is my MOA?

Coreg (carvedilol)

treats HTN, CHF, and A.Fib

antagonist at alpha1/beta receptors

Do not use with asthma

Who are am I?

I am a cardiac glycoside that is a positive inotrope inhibiting Na/K ATPase

Used to treat HTN

Who are we?

We are the anticoagulants that affect platelets

Aspirin, Plavix (clopidogrel), and Effient (prasugrel)

Persantine (dipyridamole) is a phosphodiesterase inhibitor (affects platelets)

What is my MOA?

Aspirin (acetylsalicyclic acid)

non-competitive, irreversible and non-selective inhibitor of COX 1 and 2 via covalent bonding with the enzymes active site

Inhibits Thromboxane A2

Do not give to asthma patients, or children (Reye's syndrome)

Who am I?

I am an anti-coagulant that affects platelet aggregation via non-competitve and irreversible P2y12 receptor antagonism, blocking ADP binding

Who am I?

I am used as an anti-coagulant used when patients can't convert clopidogrel to active form

What is my MOA?

Persantine (dipyridamole)

Combination phosphodiesterase inhibit and ADP receptor antagonist

when combined with aspirin= Aggrenox

can also be combined with Coumadin (warfarin)

Who are we?

We are the anti-coagulants that affect the clotting cascade

Who am I?

I block the extrinsic pathway by blocking activation of vitamin K via inhibition of vitamin K epoxide reductase

If taking me you should avoid leafy greens

Watch my INR or else

What is our MOA?

Heparin and Lovenox (enoxaparin)

covalently binds to anti-thrombin III preventing it from activating other clotting facotrs such as thrombin and factor X 

blocking the intrinsic pathway

beware of thrombocytopenia

Lovenox is used as a bridge to Coumadin (warfarin)

Who am I?

I am a direct thrombin inhibitor 

Inhibits conversion of fibrinogen to fibrin 

a pitfall is there is no antidote to my usage

What is our MOA?

Xarelto (rivaroxaban) and Eliquis (apixaban)

What is our common ending?

HMG-CoA reductase inhibitors used as lipid-lowering agents 

stimulate increased expression of hepatic LDL receptors

the "statins"

Zocor (simvastatin), Crestor (rosuvastatin), etc.

What is my MOA?

Zetia (ezetimibe)

Blocks intestinal cholesterol transporter NPC1L1 (blocking cholesterol absorption)

Used as 2nd line therapy for statin-unresponsive individuals

Who am I?

I am a combo drug of Ezetimibe and Simvastatin

I combine the inhibition of cholesterol absorption with the inhibition of choelsterol synthesis

What is our MOA?

Lopid (gemfibrozil) and TriCor (Fenofibrate)

Fibric Acid Derivatives

peroxisome proliferator-actived receptor

increases muscle expression of lipoprotein lipase, increases uptake triglyceride containing lipoproteins, increases HDL, lowers triglycerides

What is my MOA and what am I used for?

Niacin

niacin receptor agonist in adipose tissue

reduces lipase activity in adipocytes, reduces liver uptake of fatty acids, reduces production of VLDLs, raises HDL

used for high cholesterol

taking with a statin potentiates risk of rhabdomyolysis

Who am I?

I sequester bile acids allowing cholesterol to be excreted

increases liver expression of LDL receptors 

What is our MOA and what are we used for?

Lovaza and Epanova

Omega-3 Acid Ethyl Esters

inhibitor of acyl-CoA: 1,2-diacylglycerol acyltransferase, increased mitochondrial and peroxisomal beta-oxidation in the liver, decreased lipogenesis in the liver, and increased plasma lipoprotein lipase activity

Who am I and what is my usage?

I inhibit dihydrofolate reductase 

interrupting DNA, RNA, and protein syntehsis

Apoptosis of Tcells

Who am I?

I am an immunosuppresive agent that inhibits inosine monophosphate dehydrogenase

decreases lymphocyte activation/activity, induces apoptosis of Tcells, decreases expression of adhesion molcecules, decreases production of nitric oxide by PMNs

What Cytokine/Interleukin do we affect?

Cyclosporine and Prograf (tacrolimus)

What is my MOA and usage?

Prograf (tacrolimus)

calcineurin inactivation which leads to inhibition of IL-2 gene expression 

used as an immunsuppresive agent

Who am I?

I am a JAK-STAT inhibit that inhibits lymphocyte transcription 

I am used for rheumatoid arthritis as an immunsuppressant 

Who am I?

I am used to treat acute gout

I bind to tubulin and inhibit microtubule polymerization arresting cells in metaphase of mitosis. This prevents neutrophil activation, migration, and phagocytic activity

What is my MOA and what do I treat?

Zyloprim (allopurinol)

non-competitive inhibitor of xanthine oxidase which decreases the biosynthesis of uric acid precursors

used to treat chronic gout by inhibiting uric acid synthesis

Who am I?

I am used to treat chronic gout by promoting uric acid excretion by inhibiting the basolateral anion exhanger of the proximal tubule which blocks the tubular reabsorption of urate, decreasing plasma urate levels

What is my MOA and what do I treat?

Etanercept (enbrel)

Who am I?

I am used to treat rheumatoid arthritis

Monoclonal antibodies consisting of the ligand binding portion of the TNF alpha receptor

Who am I?

I am used to treat rheumatoid arthritis

I do not cure the disease, I only improve symptoms

I increase the risk for TB, fungal infections, sepsis, and CNS demyelination