Drugs

• B1 adrenergic-agonist; selective
• MOA: Beta1- increase cAMP, activation of calcium channels; primary cardiovascular effect is a rise in cardiac output as a result of increased myocardial contractility
• Use: B1- Tx of cardiogenic shock, and HF; tx of cardiac decomposition; help increase CO

• B1&2 Beta-agonist
• MOA: Beta1- increase cAMP, activation of calcium channels
• Beta2- increase cAMP [cAMP increases HR and relaxation rate]
• Use: B1- Tx of cardiogenic shock, and HF.
• B2- Tx of asthma, emphysema

• B2 Beta-agonist
• MOA: Beta2- increase cAMP [cAMP increases HR and relaxation rate]
• Use: B2- Tx of asthma, emphysema

• Phosphodiesterase
• MOA: Inhibit phosphodiesterase
• Use: Tx of HF
• Adverse Affects: Ventricular dysrhythmias

• Dopamine agonist
• MOA: Activates dopanine receptors in renal, mesenteric, and cerebral vasculature; causes vasodilation. Dopamine is a precursor for norepinephrine which activates alpha receptors.
• Use: dose dependant; Low (dopamine Rs) increased urine output, Mid (dopamine and alpha Rs) increase TPR, CVP, venous tone, High (alpha Rs) increased TPR and pulmonary resistance

• Cardiac glycosides
• MOA: Directly inhibit Na-K-ATPase, increasing intracellular Na, reducing transmembrane Na gradient reducing Ca efflux
• Use: Tx of HF
• Adverse Affects: Adecreased QT interval, Increased PR interval, ST-segment depression

• Beta-blockers
• MOA: Antagonist at B1&2 receptor; noncardioselective
• Use: Tx of hypertension
• Adverse affects: Reduced exercise tolerance; bradyarrhythmias; cardiac electrical conduction defects

• Dyhidrophyridines
• Calcium channel blockers
• MOA: Block inward flow of Ca through the slow channels of the myocytes durring phase 2 (plateau) of cardiac action potential, decreases Ca influx into smooth muscle, decreases CO, TPR, and renal blood flow; most potent vasodilator; blocks the influx of Ca into vascular smooth muscle, reducing contractility
• Use: Tx of hypertension, vasospastic angina, arrhythmias
• Adverse affects: Edema, depresses cardiac function, may cause dysrrhythmias

• Phenylalkylamines
• Calcium channel blockers
• MOA: Block inward flow of Ca through the slow channels of the myocytes durring phase 2 (plateau) of cardiac action potential, decreases Ca influx into smooth muscle, decreases CO, TPR, and renal blood flow; suppresses HR, contractility, conduction velocity
• Use: Tx of hypertension
• Adverse affects: Edema

• Venzothiazepines
• Calcium channel blockers
• MOA: Block inward flow of Ca through the slow channels of the myocytes durring phase 2 (plateau) of cardiac action potential, decreases Ca influx into smooth muscle, decreases CO, TPR, and renal blood flow
• Use: Tx of hypertension
• Adverse affects: Edema

• Calcium sensitizers
• MOA: Increase cardiac troponin Ca sensitivity, vasodilation by inhibiting PDE-III)
• Use: Tx of HF
• Adverse affects: Hypotension, reflex tachycardia

• (Vagas)
• MOA: M1 & M3 receptors, activates phospholipase, increase IP3, IP3 mediated Ca release from endoplasmic reticulum

• Vasoconstrictor
• MOA: Agonist at alpha1 adrenergic receptors, increasing smooth muscle contraction; B1&B2 in lungs, increase cAMP, phospholamban phosphorylation, Ca uptake by SR; inhibits release of ACh
• Use: Tx of life threatening hypotension not caused by hypovolemia, nasal decongestant
• Adverse affects: Increase cardiac oxygen consumption, last resort for ischemic heart disease

• (Adrenal)
• MOA: B1&B2 in lungs, increase cAMP, phospholamban phosphorylation, Ca uptake by SR; inhibits release of ACh

• Vasoconstrictor
• MOA: Agonist at alpha1 adrenergic receptors, increasing smooth muscle contraction
• Use: Tx of life threatening hypotension not caused by hypovolemia, nasal decongestant
• Adverse affects: Increase cardiac oxygen consumption, last resort for ischemic heart disease

• MOA: Alpha-1 agonist
• Use: Tx of hypertension and nasal congestion

• MOA: Alpha-2 antagonist
• Use: Tx of erectile dysfunction

• Sympatholytics
• MOA: Alpha2 agonist, inhibits vasomotor center in medulla oblongata, reducing sypathetic activity
• Use: Tx of hypertension
• Adverse affects: Can constrict corronary vessels; caution with corrinary insuficiency, recent MI, conduction disturbances

• Alpha-blockers
• MOA: Alpha1 antagonist, blocks receptor binding sites, causing vasodilation
• Use: Tx of hypertension
• Adverse affects: Othrostatic (postural) hypotension

• ACE inhibitors
• MOA: Inhibits angiotensin converting enzyme (ACE) reducing angiotensin II production, decreasing Na retension and degradation of vasodilatory prostaglandins and Nitric Oxide 
• Use: Tx of hypertension, CHF, MI
• Adverse affects: Acute renal failure, cough (due to increased bradykinin in the lungs)

• Angiotensen-II receptor blockers (ARBs)
• MOA: Antagonist at Ang II receptor
• Use: Tx of hypertension, CHF
• Adverse affects: Acute renal failure

• Nitrate vasodilator
• MOA: Increases production of nitric oxide, increasing cGMP, which inactivates MLCK in smooth muscle, causing relaxation; decreases resistance resulting in less venous return
• Use: Tx and prophylaxis of angina, Tx of CHF, MI
• Adverse affects: Hypotension

• Diuretics; 1 of 4 subclasses
• MOA: Increased renal excretion of Na and thus water, reducing plasma volume; loop diuretic
• Use: Tx of hypertension, edema, CHF, renal failure
• Adverse affects: Increased excretion of key electrolytes (Na, K, Mg, Ca)

• Diuretics; 1 of 4 subclasses
• MOA: Increased renal excretion of Na and thus water, reducing plasma volume; carbonic anhydrase inhibitor
• Use: Tx of hypertension, edema, CHF, renal failure
• Adverse affects: Increased excretion of key electrolytes (Na, K, Mg, Ca)

• Diuretics; 1 of 4 subclasses
• MOA: Increased renal excretion of Na and thus water, reducing plasma volume; thyizide
• Use: Tx of hypertension, edema, CHF, renal failure
• Adverse affects: Increased excretion of key electrolytes (Na, K, Mg, Ca)

• Diuretics; 1 of 4 subclasses
• MOA: Increased renal excretion of Na and thus water, reducing plasma volume; K-sparing agent
• Use: Tx of hypertension, edema, CHF, renal failure
• Adverse affects: Increased excretion of key electrolytes (Na, K, Mg, Ca)

MOA: Beta-1 antagonist; partial agonist; cardioselective

MOA: Beta antagonist; partial agonist; non-cardioselective

MOA: Beta antagonist; partial agonist; non-cardioselective

MOA: Beta antagonist; partial agonist; non-cardioselective

MOA: Beta-1 antagonist; cardioselective

MOA: Beta antagonist; non-cardioselective

MOA: Beta antagonist; non-cardioselective

• Prazosin: A1
• Yohimbine: A2

• Phenylephrine: A1
• Clonidine: A2

MOA: Beta antagonist; non-cardioselective

• Isoproterenol: B1&2
• Dobutamine: B1
• Terbutaline: B2

Nilrinone

Dopamine

Digoxin (foxglove)

• Cardioselective partial agonists:
• Acebutolol
• Non-cardioselective partial agonists:
• Penbutolol
• Carteolol
• Pindolol
• Cardioselective antagonists:
• Metoprolol: B1
• Atenolol
• Non-cardioselective antagonists:
• Carvedilol
• Labetolol
• Nadolol
• Propranolol

• Dyhidrophyridines: Nifedipine (vasodilator)
• Phenylalkylamines: Verapamil (suppresses HR, contractility, conduction velocity)
• Benzothiazepines: Diltiazem

Levosimendan

• Mecamylamine (nicotinic antagonist)
• Ambenonium
• Demecarium
• Pilocarpine (muscarinic agonist)
• Atropine (muscarinic antagonist)
• Tolderodine (muscarinic antagonist)

• Norepinephrine
• Noradrenaline

Clonidine

Captopril

Losartan

Nitroglycerine

• Furosemide (loop diuretic)
• Acetazolamide (carbonic anhydrase inhibitor)
• Hydroclorothiazide (thyazide)
• Spironalactone (K-sparing agent)

MOA: Inflammation mediator that actively constricts smooth muscle

MOA: Inflammation mediator that actively constricts smooth muscle

MOA: Inflammation mediator that actively constricts smooth muscle

MOA: Inflammation mediator that actively constricts smooth muscle; edema mediator that increases vascular permeability

• Inhaled and systemic; glucocorticoids and mineralocorticoids
• Beclomethasone/Beclovent (inhaled)
• Fluticasone/Flovent (inhaled)
• Prednisone (systemic)
• MOA: Anti-inflammatory or block inflammatory mediators; assist inhaled rapid acting bronchodilators used during bronchospasm
• -Glucocorticoids: Anti-inflammatory
• --Indications: Inflammatory autoimmune diseases and allergic and asthmatic diseases
• -Mineralocorticoids: Electrolyte/fluid regulation
• Use: Long-term control medication to prevent inflammation

• Corticosteroid, inhaled
• MOA: Anti-inflammatory or block inflammatory mediators; assist inhaled rapid acting bronchodilators used during bronchospasm
• Use: Long-term control medication to prevent inflammation

• Corticosteroid, inhaled
• MOA: Anti-inflammatory or block inflammatory mediators; assist inhaled rapid acting bronchodilators used during bronchospasm
• Use: Long-term control medication to prevent inflammation

• Beta-adreneric agonists: Albuterol/Proventil/Ventolin
• Anticholinergics: Ipratropium bromide/Atrovent
• MOA: Rapidly acting bronchodilator
• Use: Terminate episodes of bronchospasm

• Beta-adrenergic agonist
• MOA: Relax airway smooth muscle via B2-adrenergic receptor
• Use: Terminate episodes of bronchospasm

• Anticholinergic
• MOA: Relax airway smooth muscle by blocking muscarinic receptors
• Use: Terminate episodes of bronchospasm, not effective against allergen- or exercise-induced brochospasm
• Adverse affects: Can increase mucus viscosity and cause mucus plugging

• Mediator inhibitors: Cromolyn sodium/Intal
• Beta-adrenergic agonists: Salmeterol/Serevent
• Leukotriene antagonists: Zafirlukast/Accolate, Montelukast/Singulair
• Phosphodiesterase inhibitors: Theophylline/Theo-Dur
• MOA: Actively dilate airways
• Use: Long-term control medication to bronchodilate

• Long-acting bronchodilator, mediator inhibitor
• MOA: Actively dilate airways, prevent mast cell degranulation (histamine release)
• Use: Long-term control medication to bronchodilate

• Long-acting bronchodilator, beta-adrenergic agonist
• MOA: Actively dilate airways, relax airway smooth muscle via B2 adrenergic receptor
• Use: Long-term control medication to bronchodilate

• Long-acting bronchodilator, leukotriene antagonist
• MOA: Actively dilate airways, block leukotriene receptors
• Use: Long-term control medication to bronchodilate

• Long-acting bronchodilator, leukotriene antagonist
• MOA: Actively dilate airways, block leukotriene receptors
• Use: Long-term control medication to bronchodilate

• Long-acting bronchodilator, phosphodiesterase inhibitor
• MOA: Actively dilate airways, prevent breakdown of cAMP (activated by B2 adrenergic receptor)
• Use: Long-term control medication to bronchodilate
• Adverse affects: Require monitoring of plasma levels to prevent toxicity

• Mineralcorticoid
• MOA: Decrease inflammation by suppressing the production of inflammatory proteins and increase anti-inflammatory proteins
• Use: Reduce inflammation

• Antineoplastic agent
• MOA: Inhibits dihydrofolate reductase, which is needed to convert folic acid to tetrahydrofolic acid, which is needed for thymine production
• -Blocks DNA synthesis (rapidly dividing cells); inhibits purine metabolism (prevents protein expression)
• Use: Tx of cancer, inflammation due to decrease in cell proliferation; RA (in combo with TNF-alpha blockers) and other inflammatory autoimmune diseases

• NSAID
• MOA: Inhibits COX-1 and COX-2
• Use: Inhibit inflammation, reduce pain, fever, and headache

• Vitamin B complex (B9)
• MOA: Needed for precursor for tetraydrofolic acid to be converted to thymine
• Use: Tx of folate deficiency, megaloblastic anemia (B9 or B12 deficiency)

• Herbal
• MOA: Increase cartilage rebuilding, may draw fluid into joint
• Use: Tx of osteoarthritis

• Analgesic, NSAID, propionic acid
• MOA: Non-steroidal antiinflammatory drug (NSAID) that inhibits prostaglandin synthesis
• Use: Tx of fever, pain, headache, migraine, arthritisdysmenorrhea

• Antipyretic and analgesic
• MOA: Unknown, possibly Cox inhibitor (COX-1 and COX-2)
• Use: Reduce fever and mild pain

• Herbal
• MOA: Increase number of phagocytic cells; increase amount of proinflammatory interleukins (IL-1, IL-6, and TNF-alpha)
• Use: Immune system stimulant

• Iron Preparation
• MOA: Corrects erythropoietic abnormalities caused by an iron deficiency
• Use: Prevention and treatment of iron deficiency

• Heparins
• MOA: Neutralizes thrombin and activated factor X; prevents conversion of fibrinogen to fibrin
• Use: Prevents DVT and pulmonary embolism, prevents blood clots

• Selective Serotonin Agonist
• MOA: Binds with high affinity 5-HT type 1-like receptors; may constrict cranial blood vessels or inhibit neurogenic inflammatory processes in the CNS
• Use: Acute tx of migraine and cluster headaches

• Salicylates
• MOA: Inhibits COX-1 and COX-2; binds COX-1 irreversibly
• Use: Relief of mild pain, fever, imflammation, ischemic attack, and stroke; prevention of CAD and MI

• Beta-1 Antagonist
• MOA: Beta-1 antagonist; cardioselective; inhibits response to adrenergic stimuli by blocking receptors within the myocardium; high doses block beta-2 receptors within bronchial and vascular smooth muscle
• Use: Tx of hypertension, angina, and acute MI

• Ganglionic blocker
• MOA: Nicotinic antagonist
• Use: Tx of severe hypertension; BP control durin aortic surgery

• Cholinergic
• MOA: Inhibit acetylcholinesterase
• Use: Tx of myasthenia gravis, open angle glaucoma

• Cholinergic
• MOA: Inhibit acetylcholinesterase
• Use: Tx of myasthenia gravis, open angle glaucoma

• Cholinomimetic
• MOA: Muscarinic agonist
• Use: Tx of ocular hypertension glaucoma

• Anticholinergic
• MOA: Muscarinic antagonist
• Use: Tx of overactive bladder; reduce airway secretions during endotracheal intubation

• Anticholinergic
• MOA: Muscarinic antagonist
• Use: Tx of overactive bladder; reduce airway secretions during endotracheal intubation

• Vasodilating agent
• MOA: Relaxes arterial smooth muscle, producing vasodilation; inhibits platelet aggregation
• Use: Palliative Tx in maintaining patency of ductus arteriosus in neonates with various ductal-dependent congenital heart defects; Tx of erectile dysfunction

• Adrenals; synthetic glucocorticoids
• MOA: Systemic anti-inflammatory; immunosuppressant
• Use: (case specific) Increase respiratory function on preterm baby

• Aminopenicillin
• MOA: Inhibition of bacterial cell wall synthesis through beta-lactam
• Use: Tx of bacterial infections in the respiratory tract, UTI, and others

• Aminoglycoside
• MOA: Inhibits protein synthesis by irreversibly binding to 30S ribosomal subunit
• Use: Tx of bone and joint infections, endocarditis, and (case specific) respiratory infection

• Corticosteroid; adrenals
• MOA: Anti-inflammatory, vasoconstriction, reduces number of mediator cells and also secretion; improves lung function
• Use: Long-term prevention of bronchospasm in patients with asthma, Tx of airflow obstruction in patients with COPD
• Adverse affects: Possible adrenal insufficiency with withdrawn, glaucoma, musculoskeletal effects, category C pregnancy, immunosuppressant

• Lung surfactant
• MOA: Replaces deficient or ineffective endogenous lung surfactant in neonates with respiratory distress syndrome (RDS). Surfactant prevents the alveoli from collapsing during expiration by lowering surface tension between air and alveolar surfaces. 
• Use: Tx of neonatal RDS

• Nutritive agent, osmotherapy agent
• MOA: Source of water and carbs; minimize liver glycogen depletion and provide protein-sparing action
• Use: Tx of hypoglycemia; IV feeding

• Penicillin
• MOA: Analog of ampicillin, semi-synthetic; inhibits biosynthesis of cell wall mucopeptide; broad spectrum bactericidial activity against aerobic gram +/-; inhibit cross linking
• Use: Tx of bacterial infections

• Cyclophosphamide
• Cyclosporine A and tacrolimus (FK506)
• Rapamycin

• Cyclosporin A (FK06)
• Drugs that inhibit antibody synthesis:
• -Rapamycin
• -15-Deoxyspergualin

• Cyclophosphamide
• Methotrexate

• Alkylateing agent tageting dividing cells
• -Interstrand DNA crosslinking and intrastrand DNA crosslinking at guanine N-7
• High dose: highly toxic to all dividing cells
• -Indications: lymphomas, leukemias, some solid tumors, autoimmune diseases
• Low dose: immunomodulatory; elimination of CD4+CD2+ T regs; induction of T cell growth factors

MOA: Inhibits IL-2 driven proliferation by blocking transcription of IL-2 gene (binds calcineurin); inhibition of T cell activation by blocking Ca activation of calcineurin and then NFAT

MOA: Inhibits T cell growth; inhibits T cell responses to IL-2; not a calcineurin inhibitor

MOA: Inhibits IL-2-stimulated maturation of T cells; polarizes toward Th1 response, blocking B cell activation and antibody production