Pharm Final Review.pptx

Sources PLANT ANIMAL Alkaloids react with acids to form a salt “-ine” Hormones, enzymes, vaccines Atropine Caffeine Nicotine Morphine sulfate Insulin Oxytocin MINERA L Occur in nature or combined to yield acids, bases, or salts Sodium bicarbonate Magnesium sulfate LAB Recombinant DNA research and us...

Sources PLANT ANIMAL Alkaloids react with acids to form a salt “-ine” Hormones, enzymes, vaccines Atropine Caffeine Nicotine Morphine sulfate Insulin Oxytocin MINERA L Occur in nature or combined to yield acids, bases, or salts Sodium bicarbonate Magnesium sulfate LAB Recombinant DNA research and use of technology Fentanyl Adenosine Diazepam Medication research process Animal Testing Purpose: Evaluate a med’s pharmacologica l use, dosage ranges, and possible toxic effects Phase I Purpose: Determine the med’s pharmacokinetic s, toxicity, and safe doses in HUMANS Population: Small group of healthy volunteers Phase II Phase III Phase IV Purpose: Determine therapeutic level (toxic and side effects) Population: Small group of individuals who have the disease Purpose: Refine the usual therapeutic dose Population: Large number of diseased patients Purpose: Voluntary postmarket analysis during conditional approval by FDA DRUG PROFILE 1. NAME 2. CLASSIFICATION 3. MOA 4. PHARMACOKINETICS 5. INDICATION 6. CONTRAINDICATION 7. SE 8. ROUTE OF ADMIN 9. DOSAGE 10.HOW IS IT SUPPLIED 11.SPECIAL CONSIDERATION Names Chemic al Chemical composition and molecular structure 7-chloro-1,3dihydro-1methyl-5phenyl-2H-1,4benzodiazepin2-one Generic Official Brand Suggested by manufacturer & confirmed by United States Adopted Name Council Listed in the United States Pharmacopeia (USP) Created by manufacturer to foster brand loyalty among its customers diazepam diazepam Valium Legal regulations, standards, and legislations 1906 1914 1938 1951 Pure Food and Drug Act Harrison Narcotic Act Federal Food, Drug, and Cosmetic Empowered Act Durham Humphrey Amendment Named United States Pharmacopeia and National Formulary as official drug standards Prohibited the sale of med preps that had little/no use Restricted sale of Restricted use of addicting drugs by regulating importation, manufacture, sale, and use of opium, cocaine, and their compounds/ derivatives FDA to set and enforce premarket safety standards for drugs “Prescription Drug Amendment” Required pharmacists to have written or verbal prescriptions to dispense certain meds 1962 Kefauver Harris Amendment Required pharm manufacturers to provide proof of safety before being granted approval for marketing 1970 Comprehens ive Drug Abuse Prevention and Drug “Controlled Act Substance Act” Enforced by DEA Created the 5 Schedules of Controlled Drugs Narcotics schedules i-V 01 HIGH ABUSE POTENTIAL SEVERE DEPENDENCE *NO ACCEPTED MEDICAL INDICATION 02 HIGH ABUSE POTENTIAL SEVERE DEPENDENCE Written scripts REQUIRED; NO telephone renewals OPIUM COCAINE MORPHINE HYDROCODONE OXYCODONE 03 LESS ABUSE POTENTIAL MODERATE - LOW DEPENDENCE Scripts required to be written after 6 months or 5 refills LIMITED AMOUNTS OF OPIOIDS WITH UNCONTROLLED SUBSTANCES 04 LOW ABUSE POTENTIAL LIMITED DEPENDENCE Script required to be written after 6 months or 5 refills 05 LOWER ABUSE POTENTIAL LIMITED DEPENDENCE Dispenses as any (nonnarcotic) script HEROINE LSD BENZODIAZEPINE LIMITED AMOUNTS OF OPIOIDS FDA Pregnancy categories A Adequate studies in pregnant women have NOT demonstrated risk to fetus B Animal studies have NOT demonstrated risk but no adequate studies performed in pregnant women OR Adequate studies in pregnant women have NOT demonstrated risk to the fetus but animal studies have demonstrated adverse effects C Animal studies have demonstrated adverse effects but no adequate studies in pregnant women OR no adequate animal/pregnant women studies D Fetal risk has been demonstrated X Contraindicated in pregnant women Pharmacokinetics - absorption “Movement of meds from site of application into the body to the extracellular compartment” Factors: solubility, concentration, ph, site of absorption, surface area, blood supply at site Goal of administering a drug: ensure sufficient Increases absorption Decreases absorption BIOAVAILABILITY at target tissue in order to produce desired Enteral admin - must Parenteral admin - straight effects “survive” GI tract into the bloodstream IM admin - more vascular SubQ - less vascular Fever & Hyperthermia Shock & Hypothermia Pharmacokinetics - distribution “Movement of meds from site of absorption to site of action” Bloodstream - - - interstitial spaces - - - target cells - Fast distribution - brain, heart, kidney, liver Slower distribution - GI, skin, muscles, fat (plasma and tissue reservoir) In the vascular/lymphatic system, meds can bind with plasma protein (ALBUMIN) - Bound drug vs Free drug - Binding with plasma protein inactivates meds & prevents binding to receptor protein - ONLY non-protein bound, highly lipid-soluble meds enter blood-brain barrier Pharmacokinetics - Biotransformation “Metabolism of meds” Goal: Transform med to be a more or less active metabolite Transform med to be more water-soluble for elimination What metabolizes the meds? MICROSOMAL ENZYMES IN THE LIVER 1) oxidation - more water-soluble 2)conjugation - more polar Prodrugs(inactive) - biotransformation - activated 1st pass effect through liver may partially or completely inactivate many drugs (that is why drugs are given via IV or increase oral dose) Pharmacokinetics - elimination “Movement of meds from the tissue back into circulation, and from circulation into organs of secretion” - Kidneys - urine (glomerular filtration & tubular secretion) - Liver - bile Intestines - poop Lungs - expired air (ethanol) slower rate of elimination = med stays in the body longer PHARMACODYNAMICS 1.Drugs that act by binding to a receptor site 2.Drugs that act by changing physical properties 3.Drugs that act by chemically combining with other substances 4.Drugs that act by altering a normal metabolic pathway Agonist vs antagonist Agonist: Binds to the receptor and causes it to initiate the expected response Antagonist: Binds to a site but does not cause the (epinephrine) receptor to initiate the expected response (narcan) Agonist - Antagonist: Medication that causes the expected response but also blocks another medication from triggering the same receptor (Nalbuphine) ACTIVE TRANSPORT Mechanism that requires the use of energy to move a substance from low - high conc. Carrier-mediated diffusion Mechanism that requires the help of special “carrier” proteins to move large molecules (e.g. glucose) across the cell membrane diffusion movement of solutes from high-low conc until equilibrium on either side of cell membrane osmosis Movement of solvent (usually water) across cell membrane until equilibrium of conc on both sides of the cell membrane filtration Movement of molecules from high-low pressure (resulting from hydrostatic force) HYPERTONIC/HYPOTONIC/ISOTONIC hypotonic hypertoni c isotonic Side of Cell membrane with higher conc Side of cell membrane with lower conc Equilibrium on both sides of cell membrane COLLOIDS VS CRYSTALLOIDS colloids crystalloids Compounds of high molecular Contain only h20 weight & electrolytes Do not diffuse across cell membrane Attract water into intravascular space Plasma, albumin, dextran, hetastarch Isotonic: lactated Lactated ringer ringer soln, ns soln, ns, d5w Hypotonic: d5w 6 RIGHTS OF MED ADMIN 1. RIGHT 2. RIGHT 3. RIGHT 4. RIGHT 5. RIGHT 6. RIGHT PT MED DOSE ROUTE TIME DOCUMENTATION Parenteral DRUG ROUTES Enteral po og/ng Sl Buccal pr Iv Et Io intradermal Im Sq nasal inhaled/ nebulized Topical Transdermal umbilical 22-gauge: for fragile veins 20-gauge: for average adult (NOT for fluid replacement) 18-gauge, 16-gauge, or 14gauge: used to increase volume or to administer viscous meds (like dextrose) blood can be administered ONLY through 16-gauge or larger Catheter gauge sizes ADMINISTRATION SETS MACRODRIP: 30 gtts MICRODRIP: 60 gtts Arms, legs, and neck Central vs peripheral veins Start at distal end of the Placed near the heart For long-term use Will not collapse in hypovolemia or circulatory failure extremity and work proximally Relatively easy to perform Can collapse in hypovolemia or circulatory failure Iv complications Circulatory Pain Local infection Pyrogenic rxn Allergic rxn Catheter shear Arterial puncture overload Thrombophlebitis Thrombus formation Air embolism Necrosis Anticoagulants Iv problems - infiltration Administration of meds into surrounding tissue What does it look like? Skin coolness, local edema, leakage at site, pain, feeling of tightness ❗stop iv Iv problems - clot obstruction Clot formation “thrombus” →restart the iv using new equipment ❗do no attempt to dislodge the clot with fluid bolus Administration of io Indication When iv cannot be accessed Shock Cardiac arrest Pedi hypovolemia Contraindicati ons Fracture to tibia or femur on the side of the access Congenital bone disease Osteoporosis Definitions - i will not be writing in the definitions! Pharmacokinetics Pharmacodynamics Idiosyncrasy Tolerance Cross tolerance Tachyphylaxis Cumulative effect Drug interaction Summations Synergism Potentiation interference Definitions - i will not be writing in the definitions! Assay Bioassay Bioequivalence Teratogenic Placental barrier Blood brain barrier Therapeutic index Lethal dose Effective dose Definitions - i will not be writing in the definitions! Metabolism Biotransformation First-pass effect Receptor Affinity Efficacy 2nd messenger Onset of action Duration of action Biological half-life Medication concentration CNS Treatment of grand mal seizures Diazepam (benzodiazepine) Lorazepam benzodiazepine) Midazolam (benzodiazepine) Phenytoin (hydantoin) Phenobarbital (barbiturate) Extra pyramidal symptoms (EPS) Common SE of antipsychotic medication Muscle tremors Parkinsons-like symptoms Antidepressant meds that can cause seizures SSRI ○ tramadol Monoamine oxidase inhibitor Antidepressant classes (3) (MAOI) Tricyclic acid (TCA) inhibits reuptake of NE, serotonin, & dopamine ***TCA OVERDOSE is treated with supportive care & sodium bicarbonate (urine excretion) Selective serotonin reuptake inhibitor (SSRI) inhibits reuptake of serotonin Inhibits breakdown of the monoamine enzyme, which inhibits the destruction of Ne & serotonin ***pts taking MAOIs should not be consuming food rich in tyrosine (cheese, wine) → can cause hypertensive crisis ALPRAZOLAM (XANAX) 1. 2. 3. 4. 5. Class: benzodiazepine Mechanism of action:Indication: anxiety, panic disorder Contraindication: hypersensitivity, pregnancy SEs: poor balance/coordination, memory loss, impaired concentration 6. Dosage: 0.5 mg PO 7. NOTE: antagonist is Flumazenil ANS tHE NEURON Synapse is the gap between Action potential rapid sequence of change in voltage in membrane Depolarization - opening of na+ channels and Parasympathetic nervous system - Pupil constriction Digestive gland secretion ↓hr ↓cardiac contraction Bronchoconstriction ↑smooth muscle activity along gi tract Parasympathetic ns Cholinergic:pertaining to the neurotransmitter Parasympathomimetic:substance that PNS (cholinergic) Parasympatholytic: substances that PNS (anti-cholinergic) ACh stimulate the effects of the inhibit/block the effects of the Nicotinic ach receptors Muscarinic ach receptors Parasympathetic Receives ACh on the postganglion Receives ACh on the postganglion Adrenal medulla & Skeletal muscles Antagonist = Glands, Smooth & cardiac muscle Sympathetic nervous system - ↑secretion of sweat glands Vasoconstriction ↑blood flow to skeletal muscle ↑hr ↑cardiac contraction Bronchodilation ↑energy production - ↓blood flow to abdomen - ↓digestive activity - Smooth muscle relaxation in urinary bladder - Release of glucose stores from liver Sympathetic NS Adrenergic: pertaining to the neurotransmitter Sympathomimetic:substance that sympathetic NS (adrenergic) NE stimulate the effects of the Sympatholytic: substances that inhibit/block the actions of the sympathetic NS (anti- adrenergic) Sns - Adrenergic receptors Alpha 1 Alpha 2 Beta 1 Beta 2 ANS - alpha 1 stimulation Peripheral vasoconstriction Arteriole constriction = ↑afterload Venous constriction = ↑ preload ANS - beta 1 Stimulation: Cardiac ↑hr ↑contractility ↑conductivity ↑automaticity ANS - beta 2 Stimulation: lungs Bronchodilation Relaxation of uterine smooth muscle Ions involved in action potentials - na+, K+, ca+ Cardiac action potential Pha Rapid influx of se 0 na+ Pha K+ starts to se 1 leave the cell Pha Influx of ca++ se 2 cardia c Inotrope: change in hr Chronotrope: change in contractility Dromotrope:change in rate of impulse conduction BETA-BLOCKERS ❗ “olol” BETA-BLOCKERS → INHIBIT 𝞫1 AND 𝞫2 ADRENERGIC RECEPTORS - Reduce HR - Reduce bp - Reduce cardiac workload CALCIUM CHANNEL BLOCKERS ❗ “-IPINE” NICARDIPINE, CLEVIDIPINE, NIFEDIPINE Used for ANTIHYPERTENSIVE EMERGENCY CCB BLOCK CA++CHANNELS → DECREASED CONTRACTION OF VASCULAR SMOOTH MUSCLE & INCREASE IN ARTERIOLE DIAMETER AKA VASODILATION SODIUM CHANNEL BLOCKERS POTASSIUM CHANNEL BLOCKERS Block sodium efflux BLOCK POTASSIUM EFFLUX → slows conduction 1a → decreases repolarization 1b → increases repolarization & decreases automaticity → INCREASED REPOLARIZATION 1c → decrease repolarization & decrease cardiac contractility → INCREASED QT INTERVAL STATINS reduce LDL levels HDL carry cholesterol from peripheral tissues → liver to be broken down LDL transport cholesterol from the liver→ peripheral tissues -SLOWING DOWN LIVER’S PRODUCTION OF CHOLESTEROL ACEI Causes relaxation of smooth muscle around peripheral blood vessels → lowers systolic and diastolic bp → reduces cardiac afterload Enalaprilat (vasotec) Captopril (capoten) Thrombolytics = fibrinolytics = clot busters Streptokinase (streptase) Alteplase (tPA) Tenecteplase (TNKase) Anistreplase (Eminase) TREATMENT OF htn ANTIHYPERTENSIVES ○ BETA BLOCKERS ○ CALCIUM CHANNEL BLOCKERS ○ ACEI ○ Diuretics ○ Vasodilator Sodium nitroprusside (nitropress) Hydralazine (apresoline) Treatment of CHF Diuretics - Furosemide (Lasix), Bumetanide (Bumex) Nitro Acei - Captopril (Capoten), Enalaprilat (Vasotec) respir atory Treatment regimen for asthma 1. CORRECT HYPOXIA 2. REVERSE BRONCHOSPASM 3. TREAT INFLAMMATION 1. 2. 3. 4. 5. BRONCHODILATORS BETA 2 ANTAGONISTS METHYLXANTHINES ANTICHOLINERGICS ANTI-INFLAMMATORY AGENTS Beta 2 agonism 1.Terbutaline selective 2.Racemic epi preferred 3.Aminophyllin e - none Treatment of pulmonary edema Diuretics - Furosemide (Lasix), Bumetanide (Bumex) Nitro Acei - Captopril (Capoten), Enalaprilat (Vasotec) Dobutamine (when increased HR is not desired) Gi tract Treatment of N/V in chemo pt Ondansetron hydrochloride (zofran) Dronabinol (marinol) - cannabinoid Nabilone (cesamet) cannabinoid endoc rine ENDOCRINE SYSTEM - DIABETES “A-G-B-I” ALPHA CELLS = SECRETE GLUCAGON BETA CELLS = SECRETE INSULIN ↑ GLUCOSE IN BLOODSTREAM (HYPERTENSION) = INSULIN SECRETED ↓ GLUCOSE IN BLOODSTREAM (HYPOTENSION) = GLUCAGON SECRETED TYPE I (ONSET USUALLY IN CHILDREN) VS TYPE II (ONSET LATER IN ADULT LIFE) Glycogenolysis Gluconeogenesis Glycogen breakdown into glucose When glycogen stores are depleted: →glucagon: →lipolysis →breaks down glycogen stores from the liver →conversion of non-carbohydrate substrates to amino acids →produce glucose Synthesis of glucose →Conversion of amino acids to glucose Diabetic ketoacidosis Hyperglycemia 250-300mg/dl Usually occurs with insulin deficiency + increased glucagon activity Slow onset Polyphagia, polyuria, polydipsia Production of ketones = sweet, fruity odor from breath Kussmaul respirations Treatment: fluid administration for dehydration Hyperosmolar hyperglycemi Hyperglycemia more than c 600mg/dl nonketotic Usually Associated with type II state Super slow onset Polyphagia, polyuria, polydipsia = ↑ volume depletion NO production of ketones Treatment: fluid administration for dehydration Hypoglycemia (insulin shock) Hypoglycemia less than 80mg/dl Rapid onset Altered mental status Cold + clammy = need some candy If glucose is less than 80mg/dl ○ start iv of normal saline ○ Administer d50w iv Treatment for type 2 diabetes Oral hypoglycemics (sulfonylureas) - Diabeta Diabinese Dimelor Euglucon Mobenol orinase D50W 1. 2. 3. 4. 5. 6. 7. Class: carbohydrate Mechanism of action: supplies supplemental glucose Indication: hypoglycemia, coma of unknown origin Contraindication: none in suspected hypoglycemia SEs: tissue necrosis and phlebitis at injection site Dosage: 25 g (50 mL of 50% solution) IV NOTE: use with caution in pts with increased intracranial pressure - may increase cerebral edema GLUCAGON GLUCAGON IS A SECONDARY TREATMENT TO D50W for HYPOGLYCEMIA. GLUCAGON PROVOKES LIVER TO INITIATE GLYCOGENOLYSIS FROM THE GLYCOGEN STORAGE. IN A CACHEXIA PT, GLUCAGON WILL NOT BE EFFECTIVE BECAUSE PT HAS NOT GLYCOGEN STORAGE. Glucagon is also used to treat beta blocker & ca++channel blocker overdose acidbase Acid - base drugs OXYGEN 1. 2. 3. 4. Class: gas Mechanism of action: transported in hemoglobin of cells Indication: hypoxia Contraindication: pts that are not hypoxic - causes free radical induction and oxidative stress 5. SEs: hyperoxia 6. Dosage:depends on pt’s underlying problem 1-6 lpm 7. NOTE: Nasal cannula NRB 6-10 lpm BVM 10-15 lpm EPINEPHRINE - 𝞪 >𝞫 1. Class: sympathomimetic 2. Mechanism of action: acts directly on alpha1, beta1, beta2 receptors 3. Indication: acute asthma, anaphylaxis, cardiac arrest, severe hypotension 4. Contraindication: hypertension, tachycardia, hypertension 5. SEs: myocardial O2 demand, palpitations, tremor 6. Dosage: Anaphylaxis Cardiac arrest 0.3 mg IM 1:1000 (because you cannot put that much liquid volume via IM 1 mg IV/IO 1:10,000 7. NOTE: should be protected from light Norepinephrine 1. 2. 3. 4. 5. 6. 7. 𝞪 > 𝞫 Class: sympathetic agonist Mechanism of action: alpha and beta adrenergic stimulator Indication: hypotension Contraindication: hypersensitivity, hypovolemia SEs: bradycardia, ↑ myocardial O2 demand, N/V Dosage: 0.1-0.5 mcg/kg/min IVF NOTE: conc needs to be diluted due to potency Dopamine - 𝞪 = 𝞫 1. Class: sympathetic agonist 2. Mechanism of action: alpha,beta-1, and dopaminergic stimulator 3. Indication: hypotension, cardiac shock, bradycardia refractory to atropine 4. Contraindication: hypersensitivity, hypovolemic shock, pheochromocytoma 5. SEs: palpation, arrhythmias, CP, N/V 6. Dosage: 2-10 mcg/kg/min IVF 7. NOTE: effects based on dosage Racemic epi 1. 2. 3. 4. 5. 6. 7. 𝞪 < 𝞫 Class: sympathetic agonist Mechanism of action: alpha and beta adrenergic stimulator Indication: croup Contraindication: hypersensitivity, epiglottitis SEs: tachycardia, arrhythmia, “rebound worsening”, N/V Dosage: 0.25 - 0.75 mL IN (nebulizer) NOTE: MORPHINE 1. Class: narcotic 2. Mechanism of action: binds to opiate receptors - causes sedation and analgesia 3. Indication: severe pain 4. Contraindication: hypersensitivity, volume depleted, hypotensive, undiagnosed head or abdominal injury 5. SEs: N/V, AMS, respiratory depression 6. Dosage: 2-10 mg IV (standard dose) - additional 2 mg every few mins until pain is relieved 7. NOTE: often administered with antiemetic such as Zofran CONTRAINDICATIONS OF NARCOTICS Hypovolemic ( hemorrhage/shock/fluid depletion) narcotics can cause vasodilation Hypotension - narcotics can cause vasodilation Undiagnosed head injury - may mask the injury Undiagnosed abdominal pain - may mask the injury Hypersensitivity - may cause allergic rxn WHAT DRUG REVERSES NARCOTICS? NARCAN 1. Class: Opioid antagonist 2. Mechanism of action: competitively binds to opiate receptors in the brain 3. Indication: narcotic overdose 4. Contraindication: hypersensitivity 5. SEs: n/a 6. Dosage: 1-2 mg IV/IO/IN/nebulizer - repeat 5 mins later; 2x dosage ET 7. NOTE: can cause withdrawal symptoms in narcotic-dependant pts; only administer enough to reverse respiratory depression MORPHINE VS FENTANYL MORPHINE USUALLY ADMINISTERED WITH ANTIEMETIC AGENT, SUCH AS ZOFRAN ↑ PERIPHERAL VENOUS CAPACITANCE ↓ VENOUS RETURN ↓ MYOCARDIAL OXYGEN DEMAND FENTANYL 50-100X MORE POTENT THAN MORPHINE LESS EMETIC ACTIVITY THAN OTHER NARCOTIC ANALGESICS CAN BE ADMINISTERED INTRANASALLY USING mad DEVICE, WHICH IS PARTICULARLY USEFUL IN CHILDREN Nitroglycerin (nitrostat) 1. Class: nitrate 2. Mechanism of action: Vasodilator, 3. ↓ preload - ↓ stroke volume - ↓ cardiac output, ↑ HR 4. Indication: cp due to acute coronary syndrome or acute pulmonary edema, acute CHF 5. Contraindication: hypersensitivity, hypotension (systolic below 100 mmHg), Viagra, recent consumption of alcohol 6. SEs: tachycardia, hypotension 7. Dosage: 0.4 mg SL 8. NOTE: WHY ARE CORTICOSTEROIDS IMPORTANT in treatment of Although they are of little benefit in the initial stages anaphylaxis? of treatment, they help suppress the inflammatory response associated with these emergencies. METHYLPREDNISOLONE (SOLU-MEDROL) HYDROCORTISONE (SOLU-CORTEF) Methylprednisolone (solu-medrol) 1. 2. 3. 4. 5. 6. 7. Class: corticosteroid, anti-inflammatory Mechanism of action: inhibit substances that cause inflammation Indication: severe anaphylaxis, asthma, COPD, urticaria Contraindication: hypersensitivity SEs: fluid retention, hypertension, CHF, N/V Dosage: 125-250 mg IV/IM NOTE: effects will not be seen in pre-hospital setting due to long pharacokinetics Insulin (humulin, novolin) 1. Class: hormone, antihyperglycemic 2. Mechanism of action: combines with insulin receptors promoting glucose entry into the cell 3. Indication: hyperglycemia (type II diabetes), DKA, hyperkalemia 4. Contraindication: hypoglycemia 5. SEs: hypoglycemia 6. Dosage: 5-10 units IV - 0.1unit/kg/hr IVF, 5-20 units IM 7. NOTE: test glucose before administration; if in doubt, administer glucose (insulin is almost always administered in ED) GLUCAGON 1. Class: hormone/anti-hypoglycemic 2. Mechanism of action: causes breakdown of stored glycogen to produce glucose (also inhibits glycogenesis) 3. Indication: hypoglycemia, beta blocker overdose, calcium channel blocker overdose 4. Contraindication: hypersensitivity 5. SEs: 6. Dosage: 0.25-0.5mg IV or 1mg IM/IN 7. NOTE:secreted by alpha cells of pancreas THIAMINE (VITAMIN b) 1. Mechanism of action: required for conversion of pyruvic acid to acetyl coenzyme A (conversion of glucose to energy) 2. Indication: coma of unknown origin, especially if alcohol involved 3. Contraindication: hypersensitivity 4. SEs: hypotension, dyspnea, respiratory failure 5. Dosage: IV/IM 6. NOTE: comatose, chronic alcoholic, malnourished pts should receive thiamine in addition to glucose ATROPINE 1. 2. 3. 4. 5. 6. 7. Class: anticholinergic “parasympatholytic” Mechanism of action: blocks ACh receptors - increase HR Indication: bradycardia, organophosphate poisoning Contraindication: none in emergency situations SEs: tachycardia, dry mouth, pupil dilation Dosage: 0.5 mg IV - repeat after 5 mins (max 3 mg) NOTE: doses less than 0.5 mg can cause paradoxical slowing of the HR ORGANOPHOSPHATE POISONING S.L.U.D.G.E.M. + BRADYCARDIA SALIVATION LACRIMATION URINATION DEFECATION GI UPSET EMESIS MIOSIS Albuterol (ventolin) 1. 2. 3. 4. 5. 6. 7. Class: sympathetic agonist Mechanism of action: b2 adrenergic stimulator Indication: bronchial asthma, chronic bronchitis, emphysema Contraindication: hypersensitivity SEs: hypertension, palpation, dizziness, N/V Dosage: 2.5 mg IN (MDI or nebulizer) NOTE: What are methylxanthines? caffeine, aminophylline, theophylline MOa: block adenosine receptors??? Indications: acute bronchospasm secondary to asthma or copd Aminophylline (somophyllin) 1. Class: xanthine 2. Mechanism of action: stimulates respiratory center in the brain bronchodilation 3. Indication: bronchial asthma, chronic bronchitis, emphysema, CHF, pulmonary edema 4. Contraindication: hypersensitivity, uncontrolled arrhythmias 5. SEs: tachycardia, arrhythmia, palpitations, cp, N/V 6. Dosage: use Buretrol-type admin set ○ pt w/o fluid overload: 250 or 500 mg in 80 mL NS SLOW IVF ○ pt w/ fluid overload:250 or 500 mg in 20 mL D5W SLOW IVF LIDOCAINE 1. Class: antiarrhythmic 2. Mechanism of action: increases repolarization and decreases automaticity 3. Indication: VTach, VFib refractory to amiodarone 4. Contraindication: bradycardia, hypotension, heart blocks 5. Dosage: 1.0-1.5 mg/kg 6. NOTE: SODIUM CHANNEL BLOCKER → INCREASES THE RATE OF REPOLARIZATION → REDUCES AUTOMATICITY IN VENTRICULAR CELLS → WIDER QRS COMPLEX A ACETYLSALICYLIC ACID❗NOT - ASPIRIN CLOT BUSTER Class: platelet aggregation inhibitor, anti-inflammatory 1. 2. Mechanism of action: blocks formation of thromboxane A2 3. Indication: new cp suggestive of acute coronary syndrome, s/s of recent stroke 4. Contraindication: hypersensitivity, ulcer disease, asthma 5. SEs: GI bleed, prolonged bleeding, N/V 6. Dosage: 160-324 mg PO (chewable) 7. NOTE: early administration (within 3 hours of s/s onset of acute coronary syndrome) is associate with significantly decreased risk of death heparin 1. 2. 3. 4. 5. 6. 7. Class: anticoagulant Mechanism of action: indirect inhibitor of thrombin Indication: inhibit clot formation in acute coronary syndrome Contraindication: hypersensitivity SEs: bleeding, edema, cp, arrhythmias Dosage: 60 U/kg IV NOTE: often administered with tPA; PROTAMINE antagonizes the effects of heparin Tpa “CLOT BUSTER” 1. Class: fibrolytic 2. Mechanism of action: converts plasminogen to the plasmin enzyme (substance that dissolves clots) 3. Indication: acute coronary syndrome 4. Contraindication: bleed, cerebral lesions, recent stroke 5. SEs: bleeding, fever, N/V 6. Dosage: total 100 mg IV pump 7. NOTE: caution in pts on anticoagulation therapy ADENOSINE (adenocard) 1. Class: antiarrhythmic (class v miscellaneous) 2. Mechanism of action: decreases conduction of electrical impulse in AV node and interrupts AV reentry pathway in SVT 3. Indication: treatment of tachyarrhythmias (SVT-atria, VT-ventricles) refractory to vagal maneuver 4. Contraindication: hypersensitivity, heart blocks, asthma, afib, torsade de pointes 5. SEs: sob 6. Dosage: 6 mg rapid IV/IO bolus followed by rapid saline flush - 12 mg - 12 mg 7. NOTE: exceptionally rapid onset and short half-life (10 seconds) FUROSEMIDE (LASIX) 1. Class: Diuretic 2. Mechanism of action: inhibits sodium and chloride reabsorption into kidneys - vasodilation - decreased cardiac workload 3. Indication: adjunct to Nitro or ACEI in congestive heart failure and pulmonary edema 4. Contraindication: hypersensitivity, pregnancy 5. SEs: hypotension, volume depletion, arrhythmia 6. Dosage: 40mg (normally taking lasix) 20mg (not normally taking lasix) IV slow push 7. NOTE: can precipitate if administered with inamrinone (Incor) DIphenhydramine (BENADRYL) 1. Class: antihistamine 2. Mechanism of action: blocks histamine release (anticholinergic properties) 3. Indication: allergic rxn, anaphylaxis, EPS symptoms 4. Contraindication: hypersensitivity 5. SEs: drowsiness 6. Dosage: 25-50 mg IV/IM 7. NOTE: can also administer PO COUMADIN (WARFARIN) 1. Class: anticoagulant 2. Mechanism of action: inhibits synthesis of vitamin K 3. Indication: treatment of venous thrombosis, PE, and afib; prevention of thrombus formation 4. Contraindication: hypersensitivity, pregnancy, hemorrhage, open wounds, ulcer disease, liver disease, kidney disease, uncontrolled hypertension 5. SEs: dermal necrosis, bleeding, fever 6. Dosage: 2-5 mg PO 7. NOTE: initially developed as rat poison; antidote is vitamin K WHAT Vitamin k ANTICOAGULAN T BLOCKS THE EFFECTS IF VITAMIN K? Zidovudine (retrovir) 1. Class: HIV, Nucleotide Transcriptase Reverse Inhibitor 2. Mechanism of action: 3. Indication: HIV, AIDS 4. Contraindication: hypersensitivity, kidney disease, muscle problems, anemia, bone marrow suppression, chronic alcoholism 5. SEs: low blood count, liver problems 6. Dosage: 7. NOTE: What drugs are used to treat postpartum hemorrhage? Oxytocin (Pitocin) Terbutaline 1. Class: sympathetic agonist, tocolytic 2. Mechanism of action: beta 2 adrenergic stimulation 3. Indication: preterm labor 4. 5. 6. 7. Contraindication: hypersensitivity SEs: palpitations, anxiety, dizziness, hypertension, N/V Dosage: 0.25 mg SQ NOTE: OVERDOS E Acetaminophen Anticholinergic - “hot as hell, blind as a bat, dry as a bone, red as a beet, mad as a hatter” - iv fluids & cardiac monitoring Neuroleptics - dystonic rxn, akathisia, pseudoparkinsonism, tardive dyskinesia, neuroleptic malignant syndrome Beta blockers - glucagon Calcium channel blockers - calcium chloride or calcium gluconate Carbon monoxide - high flow o2 & hyperbaric chamber Cyanide - cyanokit (cyanocobalamin “vitamin b12”) Tca - sodium bicarbonate digoxin/digitalis - visual halos (green/yellow) - fluids & pressors Ethylene glycol Iron Isopropyl alcohol Lithium Methanol - decreased visual acuity “snowball blindness” Narcotics - supportive care takes priority over naloxone Organophosphates - atropine or 2-pam pralidoxime Salicylates “ASA” - metabolic acidosis