Drug/Application



Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|Cholinergic Agonists | |Direct Acting |Cause vasodilation by stimulating |All acetylcholine receptors are |

| | | |muscarinic type receptors on arteries |nicotinic except parasympathetic |

| | | |Increase Low viscosity saliva |end organ receptors which are |

| | | |CONTRAINDICTIONS: Bradycardia, |muscarinic |

| | | |hypotension, asthma, and peptic ulcer |1st adrenergic receptor is |

| | | | |nicotinic |

|Acetylcholine |Eye surgery - topical |Nicotinic and Muscurinic agonist | |NT as sympathetic ganglia, pre and|

| |Coronary angiography - Coronary |Broken down by AchE - Brief duration of | |post- parasympathetic ganglia, |

| |vasodilatation |action | |adrenal medulla, and NMJ |

| | |No CNS | | |

|Carbachol | |Nicotinic and Muscarinic agonist | | |

| | |NOT broken down by AchE | | |

| | |No CNS | | |

|Bethanechol |Used to stimulate intestine and |Muscarinic agonist |Decrease HR, decrease pupil diameter, |In high does - causes |

| |bladder - increase contraction and |Long duration of action |increased secretions, bronchospasms, |vasodilatation and decreased BP |

| |tone |NOT broken down by AchE |and increase GI and urinary function |due to activation of M3 receptors |

| | |No CNS | |that release NO |

|Pilocarpine |Glaucoma management - topical |Muscarinic agonist |Cholinergic crisis - salvation, | |

| |Dry mouth - oral |2 - 3 hr duration of action |lacrimination, urination, defecation, | |

| | |NOT broken down by AchE |emesis (SLUDE syndrome) | |

| | |CNS | | |

|Nicotine |Smoking cessation - patch or gum |Nicotine receptor agonist |Nicotine poisoning causes | |

| | |CNS stimulant - respiration stimulant and |depolarization block | |

| | |emetic effects |Epinephrine Effects | |

| | | |Bowel activity increase | |

|Acetylcholinesterase reversible inhibitors | |Indirect acting - temporarily blocks | | |

| | |esteratic site of AchE | | |

|Physostigmine |Antidote for atropine poisoning |CNS - restlessness and agitation | | |

| |Wide angle glaucoma | | | |

|Neostigmine |Peripheral symptoms |No CNS - due to positive charge | | |

| |Treat myasthenia gravis | | | |

| |Non-obstructive intestinal/bladder | | | |

| |atony | | | |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|Edrophonium |Diagnosis myasthenia gravis |Same as neostigmine, but shorter acting (less| | |

| | |potent) | | |

|Acetylcholinesterase irreversible inhibitor | |Indirect actine - permanently bind |Depolarization block causing |Antidote is |

| | | |respiratory failure |Pralidoxime(peripheral) / Atropine|

| | | | |(central) |

|Sarin – Nerve gas | | | | |

|Malathion (organophosphates) – pesticide |Treat lice | | |Penetrate CNS |

| | | | |Humans break |

|Isoflourophate |Glaucoma - not a first line drug |Duration of action - 1 week |Overuse leads to toxicity (SLUD) | |

|Acetylcholinesterase reactivator | | | | |

|Pralidoxime |Antidote for AchE inhibitor |Reactivates AchE - only effective if given | |Peripheral antidote |

| | |early | | |

| | |No CNS - positive charge | | |

|Acetylcholine receptor antagonist | | |Muscarinic antagonist side effects: | |

|Atropine - from belladonna or jimson weed |Treat Parkinson |CNS |Dry mouth | |

|plants |Treat intestinal spasms |Muscarinic antagonist |Constipation | |

| |Best treatment for organophosphate | |Decreased sweating | |

| |poisoning | |Mydriasis | |

| |Decrease nasal secretions | |Urinary retention | |

| |Dilate eye to examine the retina | |Tachycardia | |

| |Acute iritis | |Decreased tears | |

| |Physostgimine poisoning | |Precipitation of glaucoma | |

| |Bronchodilation (no longer used) | |Decreased respiratory secretions | |

|Scopolamine - from belladonna plant |Treats motion sickness |Increase CNS effect | |Drowsiness |

| | |Muscarinic antagonist | |Amnesia |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|Ipratropium |COPD w/o dryness, bronchial dilation |NO CNS | |Do NOT block the direct effect of |

| | |Muscarinic antagonist | |various mediators in asthma that |

| | |Decreases vagal tone - the important | |act directly on airway smooth |

| | |bronchoconstrictor mechanism | |muscle |

| | |Onset (15 - 30 min), peak (1 - 2 hrs), | |Effective in pts. With COPD |

| | |duration (6 - 8 hrs) | |Muscarinic antagonist + B aginist |

| | | | |= 1st line defense in COPD |

| Trimethaphan/ Mecamylamine |None currently-was used to lower BP in|Nicotinic ganglia specific |Constipation | |

| |Hypertensive crisis | |Atony of bladder | |

| | | |Cycloplegia | |

| | | |Decreased sweating | |

| | | |Postural hypotension | |

| | | |Increased HR | |

|Shock Management | | | |Catecholamines must be given IV |

| | | | |due to 1st pass metabolism |

| Dopamine |Low doses – D1 |D1, (1, (1 | |Used via IV |

| |Moderate - (1 |Brief duration - inactivated by liver MAO | | |

| |High - (1 | | | |

| Epinephrine |Dose dependent |(1 (2 (1 (2 Agonist |Vasoconstrictor - do NOT use at | |

| |Cardiac stimulant (B1) | |terminal arteries | |

| |Bronchodilator (B2) | | | |

| |Glaucoma (A1) | | | |

| |Given IV, topical, inhalation | | | |

| Norepinephrine |Infrequently used - increases BP and |(1 (2 (1 Agonist |Constricts renal blood flow | |

| |contractility |NO CNS | | |

| |Given IV | | | |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

| Phenylephrine |To treat paroxysmal super ventricular |(1 Agonist - vasocontriction | | |

| |tachycardia | | | |

| |Induces vagally mediated reflex | | | |

| |Decrease nasal secretions - topical | | | |

| |Induce mydriasis - does NOT effect | | | |

| |accommodation | | | |

|Indirect acting Sympathomimetics | | | | |

|Ephedrine |Used orally |Release of NE |Relax bronchial muscle |Herbal supplement |

| |Weight loss |B2 receptor agonist (minimum) |Vasoconstriction of vessels in nasal | |

| |Performance enhancement |CNS stimulant |mucose | |

| | | |Increased HR and BP | |

| | | |Actions blocked by: cocaine (block | |

| | | |uptake), TCA (block uptake, and | |

| | | |respirine (deplete NE content) | |

|Amphetamine |Narcolepsy |Catecholamine release |Increased BP and HR | |

| |Hyperactivity in children |CNS stimulant | | |

| |Appetite control | | | |

|Cocaine |Vasoconstriction |α2 adrenergic agonist-blocks re-uptake of |Increase BP and HR | |

| |Local anesthetic in surgical |serotonin, dopamine, and Norepinephrine |Highly Addictive | |

| |procedures |CNS stimulant | | |

| | |Produces a massive release of DA | | |

|Diuretics |HTN | |Fluid and electrolyte imbalance | |

| |Nephrogenic diabetes insipidus | | | |

| |Hypercalcemia | | | |

| |Hypercalciuria | | | |

|Mannitol |Transiently control cerebral edema |Osmotic diuretic (inert sugar) |Dehydration |Used in IV |

| |during neurosurgery |Loop of Henle |Hypernatremia | |

| |Maintain renal blood flow during major|Increases delivery of Na and water out of |Temporary volume expansion | |

| |vessel surgery |the loop into the blood - decreases |CONTRAINDICTIONS: Pulmonary edema, | |

| |Manage drug interactions |viscosity |anuria, dehydration | |

| | |Expands ECF volume | | |

| | |Decreases renin release | | |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|Acetazolamide |Glaucoma |Inhibits carbonic anhydrase - both membrane|Causes metabolic acidosis |Rarely used as a diuretic |

| |Antiepileptic |bound and cytoplasmic CA |CONTRAINDICTION: Sulfa drug allergy | |

| |Prevention of altitude sickness |Increase urinary HCO3 excretion | | |

| | |Increased Na and Cl delivery to the loop of| | |

| | |Henle | | |

|Thiazides (Hydrochlorothiazide) |Edema states |Inhibits the Na, Cl symport |Chronic use decreases Ca excretion |Less efficacious than loop |

| |HTN |Distal tubule | |diuretic |

| |Nephrogenic diabetes insipidus | | | |

|Loop Diuretics |Mobilize edema fluid |Ascending loop |Dehydration |K+ Wasting (does not require |

|Furosemide |Via IV - pulmonary edema |Inhibits the Na-K-2Cl transport |Hyponatremia |supplement) |

|Ethacrynic acid |Hypercalcemia |Increase excreation of Ca, Mg, Na, Cl |Hypernatremia | |

| | | |Hyopkalemia | |

| | | |Ototoxicity (deafness) | |

| | | |CONTRAINDICTION: Sulfa drug allergy, | |

| | | |hypercalciuria, calcium kidney stones | |

|Spironlactone |Refractory edema associated with |Aldosterone receptor antagonist |Hyperkalemia |K sparing |

| |secondary hyperaldosteronism |Late distal and collecting ducts | | |

| |HTN and edema | | | |

| |Primary hyperaldosteronism | | | |

| |Co-administered with loop diuretics | | | |

| |and thiazides | | | |

|Triamterene |Used with loop diuretics and thiazides|Inhibit Na channels |Hyperkalemia |K sparing |

| | |Late distal and collecting ducts | | |

|B agonist | | | | |

| Dobutamine |Stimulate heart in cardiogenic shock |(1 Agonist | | |

| |Short term - cardiac decomensation | | | |

| Abuterol (metaproterenol) |Dilate bronchial airways - used to |(2 Agonist |Given orally - decrease BP and increase| |

| |manage asthma, COPD | |HR | |

| | | |Given via inhalation - jitters and | |

| | | |tremors | |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|Isoproterenol |Mild or transient episodes of heart |(1 (2 Agonist |Tachycardia | |

| |block | | | |

| |For cardiac arrest until cardioversion| | | |

| |can be performed | | | |

| |Bronchodilator (minimum) | | | |

|(-Blockers (Sympatholytic drugs) |HTN |Chronic use (months) - Increased ejection |DO NOT use with asthma patients, COPD, |Gradual removal due to |

| |Cardiac arrhythmias (AF - after |fraction, contractility, and improvement in|unstable CHF, Occlusive peripheral |upregulation of receptors |

| |cardiac inversion) |systolic performance with decrease in |vascular disease |In persons with mild, moderate, or|

| |Angina |systolic and diastolic volumes and left |Can cause AV Heart block |severe heart failure - reduces |

| | |ventricular mass |High Doses |morbidity (40%) and mortality |

| | | |With Ca+ blockers |(30%) |

| | | |With Digoxin |Use with ACE inhibitor when |

| | | | |treating CHF |

|Propanolol |Management of |(1 (2 –Antagonist (non-selective) - |Bad dreams | |

| |Hypertension |Decrease cardiac work and CO |Depression | |

| |Angina |Blocks renal (1 receptors to inhibit renin |Sexual dysfunction | |

| |Cardiac arrhythmias |release - decrease angiotensin |Aggravation of severe congestive heart | |

| |Migraine headaches |No ISA |failure and occlusive peripheral | |

| |Anxiety | |vascular disease | |

| | | |Bronchospasms in asthma and COPD | |

| | | |INTERACTION: Calcium channel blockers | |

| | | |and Digoxin - causes AV block | |

|Metoprolol |Hypertension |(1 –Antagonist - selective |SEE ABOVE |SEE ABOVE |

| | |No ISA | | |

| | |Decreases CO and renin | | |

|Timolol |Glaucoma (major use) |(1 (2 –Antagonist | |topical |

| |Antiarrythmia |Decrease IOP by decreasing aqueous humor | | |

| |Treat hypertension |production | | |

|Central (-Agonists | | | | |

|Clonidine |Centrally acting Anti-Hypertensive |(2-Agonists |Sedation |If given IV can cause direct |

| |(oral) |Inhibits release of NE - acts |Withdrawal hypertension |vasoconstriction via A2 receptors |

| | |pre-synaptically |Decrease libido | |

| | |Decreased sympathetic outflow to the heart-| | |

| | |Decreased CO |Rebound hypertension | |

| | |CNS | | |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|(1-Blockers | | | | |

| Phentolamine (Regitine) |Lowers BP and HR of pheochromacytoma |Competitive antagonist for both (1 (2 |Tachycardia | |

| |Raynaud's diseases (vasospasms) |receptors | | |

| |Erectile dysfunction | | | |

| Prazosin |Lowers BP - not widely used |(1-Antagonist |Postural Hypotension |Initiate with lower dose |

| |BPH - relax bladder smooth muscle |Decrease on total peripheral resistance |Syncope - 1st full dose |Give at night |

| | |Increase in venous capacitance |Favorable lipid shifts | |

|Vasodilators | | | | |

|Hydralazine |Hypertension (not 1st line) |Direct SM relaxation by decrease in Ca and |Baroreceptors may cause tackycardia and| |

| |Reduce afterload in the treatment of |increase in NO |increase oxygen usage (Blocked by | |

| |heart failure when ACE inhibitors |Decrease in TPR |B-blockers) | |

| |cannot be used | |Immunogenic - Slow acetylators develop | |

| | | |lupus like symptoms | |

|Minoxidil |Hypertension - drug resistant |Activates ATP dependent K channels |Barrow receptors may cause tackycardia |USE in combination with (-Blockers|

| | |resulting in hype-polarization and |and increase oxygen usage |and diuretics |

| | |relaxation of SM |Tachycardia | |

| | |Decrease in TPR |Pericardial effusion | |

| | | |Fluid retention | |

| | | |Hypertrichosis (xs. hair) | |

|Sodium Nitroprusside |Hypertension Crisis - via IV |Fe-cyanide complex |Hypotension |Use only in patients with NORMAL |

| | |Increases release of NO - activates |Cyanide and thiocyanate poisoning |liver and kidney function so |

| | |guanylcyclase ( cGMP ( relax SM | |toxins can be metabolized and |

| | |Decrease in cardiac preload and afterload | |eliminated |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|Nitroglycerin |Sublingual - venodilatation in the |Releases NO upon contact |Hypotension |Develop tolerance |

| |peripheral, splanchic, and pulmonary |Decreased venous return (preload) ( |Decrease cardiac output |Use: sublingual, topical, buccal, |

| |vascular beds |decrease volume ( decreased contractility (|Syncope |oral spray, IV |

| |IV or high dose –decrease afterload |decreased oxygen consumption |Headache |Short duration of action |

| |Abort acute angina attacks |Slight arteriolar dilatation |Possible dependence | |

| |Angian prophylaxis |Dilatation of epicardial coronary a. and of|CONTRAINDICTION- Sildenafil (Viagra) - | |

| | |the collaterals ( blood flow shifts to |increased vasodilation effect due to | |

| | |ischemic areas even though there is a |increased amount of cGMP | |

| | |decline in overall flow | | |

|Isosorbide dinitrate |Angina prophylaxis |Releases NO - long acting |CONTRAINDICTION- Sildenafil (Viagra) - |Sublingual, chewed, or swallowed |

| |Heart failure - decreases preload | |increased vasodilation effect due to | |

| | | |increased amount of cGMP | |

|Sildenafil (Viagra) |Erectile dysfunction |Inhibits phosphodiesterase-type 5 |Increases effects of NO | |

| | |Inhibits the degradation of cGMP - |Hypotension | |

| | |vasodilation | | |

|ACE Inhibitors | | | | |

|Captopril |Management of hypertension |Inhibits ACE |Hypotension on first dose |Reduces mortality by 25% |

| |CHF |Inhibits ACE from degrading vasodilator |Renal insufficiency w/arterial stenosis| |

| |Postmyocardial infarction not treated |bradykinin |due to efferent arteriole relaxation, | |

| |with thrombolytics |Indirectly inhibits Angiotensin II from |therefore decrease in GFR | |

| |Ejection fraction is 50 sec and |

| |Cardiopulmonary bypass | |Thrombocyopenia |PTT - heparin plasma [0.2 - 0.4 |

| |DVT (IV) and DVT prevention (subcu) | |Arterial thromboembolism |U/ml) |

| |PE and PE prevention | |Hypersensitivity |IV Only |

| | | |Osteoporosis |Does NOT cross placenta |

|Unfractionated (UFH) |Initial treatment for |Enhances antithrombin III and IIa, which |Heparin induced thrombocytopenia (HIT) |OK for breast feeding or pregnancy|

| |DVT |deactivates Thrombin and Factors Xa and Iia |- Activates antiplatelet Ab (IgG) that |Widespread binding - unpredictable|

| |PE |Short half-life (0.5 - 1 hour) |activate platelets via their Fc Iia | |

| | | |receptors | |

|Low molecular weight |Subcutaneous b.i.d |Enhances antithrombin IIIa only, which |Spinal or epidural hematoma |Predictable |

|(LMWH) |DVT - prophylaxis |deactivates factor Xa more than Iia |Less likely: HIT, but if already HIT |↑ ½ life, ↑ bioavailability |

| |Venous thromboembolism |Long half-life (4 - 6 hours) |DON’T use | |

| | |Eliminated in kidney | | |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

| Warfarin - Oral |DVT - begin during heparin treatment |Interferes with vit K therefore reducing |Hemorrage |½ life 35-45 hrs |

| |PE - begin during heparin treatment |factors VII, IX, X, and Thrombin |Teratogenic - CROSSES placenta |Therapeutic delay (3-4 days) |

| |Atrial fibrillation |Long duration (35-45 hrs) |CONTRAINDICTIONS: Rifampin - increases |PT or INR 2-3 |

| |Acute MI |Metabolized by cytochrome P-450 |metabolism; Nafcillin - loss of |Treat OD with Vit K |

| |Valvular heart disease | |activity; alcohol - chronic: decrease | |

| |Recurrent systemic embolism | |activity, acute: increased; | |

| | | |Metronidazole, trimethoprim, and | |

| | | |sulfamethoxazole - decreases metabolism| |

| | | |of S isomer; Amiodarone - decreases | |

| | | |metabolism of S and R isomer; Aspirin -| |

| | | |risk of bleeding | |

|Protamine Sulfate |Reversal of Heparin's (LMWH) actions |Basic protein that binds the acidic heparin | |Partially reveses the anti-factor |

| | |to for a stable compound | |Xa activity |

|Vitamin K |Reverse warfarin's anticoagulant |In the process of carboxylation of Factors | | |

| |effects |Vii, IX, X and thrombin, vit. K is oxidized | | |

| | |to am epoxide - a required step | | |

|Pulmonary | | |All (2 agonists |Asthma: |

| | | |Palpitations (2 dilation which leads to|1) Mild-Albuterol |

| | | |barrow receptors increasing HR |2) Low dose ICS |

| | | |Tremor – caused by stimulation of (2 in|3) Low - Med dose ICS + LABA |

| | | |skeletal muscles - Na-K ATPase causing|4) High dose ICS + LABA |

| | | |hypokalemia |COPD: |

| | | | |1st line- B agonist + |

| | | | |anticholinergic bronchodilators |

| | | | |Symptomatic -ICS |

| | | | |Acute exacerbation -inhales B |

| | | | |agonist and anticholinergic, plus |

| | | | |systemic CS |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

| Abuterol (metaproterenol) |Bronchodilator - inhalation |(2 Agonist |Tremors - B2 receptors on skeletal | |

| |Acute attacks |Activates adenylyl cyclase ( increased cAMP (|muscle | |

| | |PKA ( relaxation of smooth muscle |Palpitations - B2 receptors on | |

| | |Duration of action 3 - 6hr |peripheral vasculature ( vasodilatation| |

| | | |( reflex- increased cardiac force and | |

| | | |rate of contraction | |

| | | |Hypokalemia - stimulate K+ uptake by | |

| | | |skeletal muscle via muscle Na-K-ATPase | |

| | | |pump ( cardiac arrhythmias | |

| Salmeterol |Bronchodilator - prevention of |Long Lasting B2 Agonist | |Should NOT be repeated for acute |

| |attacks, b.i.d. |Long duration >12 hrs | |attacks |

| Theophylline (Caffeine) |2nd line therapy for COPD and asthma |Methylxanthine compound |Common side effects- nausea, tremor, |Conditions that decreased |

| |Must be monitored |Unclear mechanism - results in smooth muscle |HA, agitation, and insomnia |elimination: |

| |5-15 mcg/ml therapeutic range; 30 |relaxation, improved diaphragmatic |Severe toxicity > 30 mcg -Seizures, |CHF |

| |mcg/ml toxic range |contraction, and increased mucociliary |arrhythmias |Liver disease |

| |In elderly and pts. with COPD - max |clearance | |Cor pulmonale - increased |

| |12 mcg/ml |Some anti-inflammatory effects | |pulmonary a. pressure |

| | |Well absorbed for GI tract | |Ciprofloxacin |

| | |Volume of distribution: 0.5L/KG | |Erythromycin |

| | |- 1mg/kg increases 2mcg/ml | |Conditions that increase |

| | |Clearance varies among and within individuals| |Elimination |

| | |- cleared by cytochrome p450 in liver | |Smoking |

|Corticosteroids |Asthma |Binds to GC receptor in cytoplasm and enters |See below for specifics | |

| |COPD |nucleus | | |

| |Rhinitis - use topically |Forms homodimer and binds to GRE - results in| | |

| |See below for specifics |transcriptional regulation of specific target| | |

| | |genes | | |

Drug/Application Clinical Mechanism Drug Interactions/ Comments

Uses Side Effects

|Prednisone |COPD - acute excerbations |Oral corticosteroids - systemic |CHRONIC EFFFECTS |Inhaled w/precautions avoid most |

| |Asthma |Binds to GC receptor in cytoplasm and enters |Adrenal insufficiency |if not all side effects |

| |Give twice daily |nucleus |Glucose intolerance |20% reaches respiratory tract when|

| |Good on: |Forms homodimer and binds to GRE - results in|Osteoporosis?Compression fractures |inhaled |

| |Sneezing |transcriptional regulation of specific target|Myopathy - esp. quads |Osteoporosis is treated by |

| |Rhinorrhea |genes |Osteonecrosis |bisphosphonate /Ca++ |

| |Pruritis | |Cataracts | |

| |Nasal Blockage | |Glaucoma | |

| | | |Psychosis | |

| | | |Cushingoid appearance | |

| | | |Obesity | |

| | | |Hypokalemia | |

| | | |Immune Suppression/ infection | |

| | | |Purpura | |

| | | |Delayed wound healing | |

| | | |In children - stunted growth | |

| Beclomethasone |1st line therapy in asthma |Inhaled corticosteroid - same mechanism as |Limited systemic effects |Use of spacer limits amount |

| |Symptomatic COPD - chronic use |above |Oropharyngeal candidias (thrush) |deposited in the oropharynx (nl. |

| | ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download