Ch 1 The Nursing Process and Drug therapy

five phases of the nursing process. 1. Assessment- Data collection involves both Subjective and Objective. Should be focused on symptoms & organs most likely to be affected by clients drug therapy - Subjective- Current Healthy history, client verbalized symptoms, current medications (dosage, route, frequency, & prescribing physician), clients knowledge of their medications, drug allergies, clients compliance of drug regimen, over the counter supplements, past medical history, clients environment, and their support system. - Objective Gross and fine motor movement, ROM, laboratory results, diagnostic studies, clients height weight and other physical assessment values temperature, pulse, blood pressure and respirations. 2. Diagnosis -human response to illness (actual or at risk) -related to -as evidenced by 3. Planning- Setting of the goals for the patient and developing interventions to help patient to accomplish them. 1. Goals should always follow SAME: 2. Specific for this patient 3. Action oriented 4. Measurable ( and in a specific time frame) 5. Evaluation- is able to continually be evaluated and revised as necessary. 4. Implementation- this would be our Nursing actions 5. Evaluation REMEMBER OUR NURSING RESPONSIBILITY IS TEACHING ! 5 Big Ones: each and every time Right Patient Right Drug Right Dose Right Time Right Route Right Documentation (the 6th) Right Rationale Right to Refuse Nursing responsibilities of medication administration One of key interventions in nursing care. Name of drug Intended use Effects on body Contraindications and precautions Special considerations Why it is prescribed How to administer the drug

Ch 2 Drug Action

Pharmacology: The study of drugs and their interactions with living systems Encompasses the study of the physical and chemical properties of drugs as well as their biochemical and physiological effects. Clinical Pharmacology: Study of drugs in humans (includes study of drugs in patients as well as healthy volunteers). DRUGS: Effectiveness: Most important! Elicits the response for which the drug is given. Current US law requires proof effectiveness prior to release for marketing. Safety: One that cannot produce harmful effects (there is no such thing as a SAFE drug) Selectivity: Elicits only the response for which it is given thus no side effects (No such thing as a selective drug). Pharmacotherapeutics: The medical use of drugs (use to dx, prevent or treat disease, or prevent pregnancy) Pharmacokinetics: The study of the movement of drugs through the body. Drugs that are taken by mouth go through three phases A PO drug has to become a solution so that it can pass through biological membrane. This process is called dissolution. If a drug is administered intravenously, intramuscularly or subcutaneously there is no dissolution Four Basic Processes 1. Absorption (think stomach) 2. Distribution (think blood flow) 3. Metabolism (think liver) 4. Excretion (think kidney) Movement through the body Absorption: the movement of a drug from its site of administration into the blood. -Enhanced absorption occurs by rapid drug dissolution, high lipid solubility, a large surface area, and high blood flow at the site of administration. Distribution: defined as the movement of drugs throughout the body. - In most tissues, drugs can easily leave the vasculature through spaces between the cells that compose the capillary wall. - Many drugs reversibly bind to albumin. While bound to albumin, drug molecules cannot leave the vascular system. Metabolism: Biotransformation. Enzymatic alteration of drug struction -most takes place in the liver and is catalyzed by cytochrome p450 system of enzymes. -Most important consequence of drug metabolism is promotion of renal drug excretion First-Pass Effect: rapid inactivation of some oral drugs as they pass through the liver after being absorbed. Essentially, how much drug is left available after passing through the liver. Used to determine dosage and intensity. Excretion: Most drugs are excreted by the kidney. -Renal drug exretion has 3-steps: glomerular filtration, passive tubular

reabsortion, and active tubular secretion. -Drugs that are highly lipid soluble cannot be reabsorbed back into the kidney -Drugs can be excreted into breast milk. Bioavailabilty: free-circulating drug system (post-first pass) even after binding. Half-Life: Time required for the amount of drug in the body to decline by 50%. Shorter the half-life, the more frequent the administration. Time to reach plateau about 4 half-lives. Drugs with a long half-life may need a loading dose to reach plateau. Pharmacokincetic tolerance: results from a accelerated drug metabolism. Pharmacodynamics: Is the study of drug concentration and its effect on body. Drug response can be primary effect or a secondary physiological effect. -Think Onset of action-Is the time it takes the drug to reach minimum effect concentration -Time of Peak effect of the drug -Time that it takes for drug to reach its highest blood or plasma level -Duration- The length of time the drug has a pharmacological effect. Agonist: Drugs that produce a response Antagonist: Drugs that inhibit/block a response Categories : There are four 1. Stimulation/or Depression- either the drug stimulates of depresses a cell or a glands activity. 2. Replacement- drug replaces an essential body compound like insulin 3. Inhibition or killing of Organism- think antibacterial or anti- fungal agents 4. Irritation-here think of laxatives causing intestinal irritation to stimulate peristalsis. Reducing risk of adverse interactions: minimize # of drugs the patient is on. Take a thorough drug history. Adjust dosages when using an inducing agent. Adjust timing of administration to reduce absorption problems. Monitor for early signs of toxicity. Be vigilant when a patient is on a drug with a low therapeutic index. Pharmacodynamic tolerance: results from adaptive changes that occur in response to prolonged exposure. It increases the MEC of a drug.

is

Therapeutic Index: (LD50: ED50) A measure of a drugs safety. Drugs with a high TI are presumably safe. Enteral Drug Administration Advantages/Disadvantages Convenient and least costly Safe

Can be a fast absorption Sublingual has a rapid onset Swallowing difficulties can make it difficult in some people May be inactivated if tablets or capsules crushed or opened Can irritate mucosa Can be inactivated by enzymes or hepatic circulation Depends on client gastrointestinal motility and mobility Parenteral Drug Administration Advantages/Disadvantages Rapidly absorbed Rapid onset of action Not inactivated by enzymes or metabolized in liver Possibility of introduction of pathogenic microbes Once injected, cannot be retrieved Topical Drug Administration Advantages/Disadvantages Fewer side effects Absorbed slowly but consistently Rectal safe for comatose clients Unless ordered, not applied to compromised skin Rectal route may be difficult to retain Can work locally, or be absorbed for generalized body use Example triamcinolone vs. fentanyl Multidrug Therapy and Drug Interactions Additive effect : 1 + 1 = 2 Synergistic effect : 1 + 1 = 3 Antagonistic effect : 1 + 1 = <1
Ch 3 Life Span

Considerations pregnancy, breast feeding, neonatal, pediatric, and elderly

-Pregnancy -first trimester greatest risk of drug induced developmental defects -last trimester, greatest percentage of maternally absorbed drugs get into fetus

-neonatal, pediatric considerations

-Best way to calculate drug dose is body surface area -Elderly Ch 4

FDA Drug Approval Process: Preclinical testing (in anmials) toxicity Pharmacokinetics Possible Useful effects | Investigational New Drug (IND) Status | Clinical Testing (in humans)

Phase I subjects: normal volunteers ; tests: metabolism and biologic effects | Phase II subjects: patients ; tests: therapeutic utility and dosage range | Phase III subjects: patients ; tests: safety and effectiveness | Conditional Approval of New Drug Application (NDA) | Phase IV: postmarketing Surveillance
Ch 6-10

Allergic Drug Reaction: an immune response. Estimated <10% of adverse reaction are allergice type. Intensity of reaction is dependent on degree of immune sensitization not dose size. Medication Errors: Any preventable event that may cause or lead to inappropriate medication use or patient harm, while the medication is in the control of the healthcare professional, patient, or consumer Medication Errors: Major cause of morbidity and mortality. Can be made by many people, incuding pharmaceutic workers, pharmacists, physicians, transcriptionists, nurses, patients and patients families. 3 Common types of Fatal Med Errors: Human factor, Miscommunication, Confusion caused by similarities in drug names. (Others include packaging, formulations, delivery devices, labeling and reference materials). Effective measures for reducing med Errors: using safety checklist for high alert drugs. Replacing handwritten med orders with computerized order entry system. Having a clinical pharmacist accompany ICU docs on rounds. Avoid error-prone abbreviations. Use a computer bar-code system.
Reporting med errors: report to prescriber and nursing management, document error per policy and percedure, factual documentation only Ch 14 CNS

CNS depressants benzodiazepines "lam & pam" Temazepam used to treat insomnia & to decrease nocturnal awakenings short term use Give at BEDTIME check for signs of reparatory distress. AVOID ALCOHOL & other CNS depressants SE: hangover, light-headedness, dizziness, or confusion overdose: administer an EMETIC and follow w/activated charcoal/conscious pt or gastric lavage/unconscious pt administer ROMAZICON has sedative effect Central acting muscle relaxants SOMA Flexeril Skelaxin used for muscle spasms, diseases, involuntary motor activity. Depresses CNS. SE: drowsiness, NO ALCOHOL! taper off dont stop abruptly. SHORT term 3 weeks or less.

Take w/ food

Ch 36 Antihistamines, Decongeststants, Antitussives, and Expectorants Antihistamines - drugs that directly compete for histamine for specific receptor sites Two types - H1 1nd H2 H1 antagonist (antihistamine) Examples - diphenhydramine (benadryl, loratadine (Claritin Properties - Antihistaminic, Anticholinergic, Sedative H2 blockers or H2 antagonisrs Used to reduce gastric acid in pepti ulcer disease Examplescimetidine (tagament), ranitidine (zantac), famotidine (pepcid) Histamine-mediated disorders - allergic rhinitis, anaphylaxis, angioneurotic edema Histamine vs. antihistamine, cardiovascular Histamine effect - dilation and increased permeability Antihistamine - reduces dilation of blood vessels, reduces permeability of blood vessels Antihistamine(H1 blockers) Benadryl (newer: Claritin, ALLEGRA(more specific) compete for hystamine receptor site to decrease nasopharyngeal secretions. have anticholinergic properties:(urinary retention, dry secretions, dry mouth). CAUTION with BPH and GLAUCOMA. SE: drowsiness. for acute asthmatic attack, respiratory; also allergic reactions, prevents motion sickness, sleep aid and antitussive. depress CNS DONT take with ALCOHOL, narcotics Use BEFORE allergy onset. SE:ARRYTHMIAS, sedationthick secretions...ALWAYS assess pt for urinary retention PRIOR to starting therapy H2 blockers Tagamet Zantac Pepcid Axid BETTER histamine receptors antagonist .used to prevent and treat ulcers and GERD. decreases gastric acid secretion by inhibitingH2 receptors in stomach. take PRIOR to Meal and at bedtime. SE: HA, dizziness, constipation, skin rash, gynecomastia (enlrged breast in male)stop drug and it goes away, impotence(reversible)

Antitussive narcotic: CODEINE over the counter: DEXTROMETHORPHAN suppresses cough reflex. if cough is nonproductive and irritating: can give antitussive. productive cough may be useful. GIVE AFTER MEALS!!!! ugH2 (histamine2) smooth muscle contraction and capillary dilation. 3. Result: Antihistamines. A. Mechanism of action.

1. Allergic reaction - histamine release 2. Histamine1 (H1) stimulation - bronchoconstriction, itching, stomach upset. P Preventative anti inflammatory Flovent Singulair(inflammation to lungs) inhaled corticosteroid: take daily. rinse mouth after using to prevent thrush. NSAID inhaler for prevention. effective in reducing inflammatory symptoms of asthma triggered by allergic and environmental stimuli. these groups recommended for acute asthma attack inhaler shake 1st wait 1 min between puffs rinse mouth after steroid inhaler Corticostreoids PREDNISONE to decrease inflammation. cortisone can get shots. DEXAMETHASONE: for inflammation of the brain. used for inflammation conditions(autoimmune disorders),allergy, prevents organ rejections. Monitor: VS, BP, wt., blood glucose, electrolytes, ECG Cushing-like symptoms...buffalo hump, sodium elimination SE" HA,HYPERglycemia, increase in BP, HR, appetite. not healing quickly. GI upset. ups SODIUM and GLUCOSE...lowers Potassium and Calcium. SE: muscle wasting, mood changes, demineralization of bones methylxanthine class Theo dur Pts. with COPD. acts like caffeine. stimulates SNS: bronchodilation. smooth muscle relaxant of respiratory system: opens airways. used for asthma, COPD. Stimulates CNS, leads to diuresis, tremors, dysrthmias. narrow therapeutic(10-20mcg)monitor serum level. give IV slowly! smoking increases metabolismof drug: smokers need higher doses. ASSEESS lungs! maintain hydration, avoid caffeine! assess cardiac and CNS response(dysrythmias, HTN, tremors

Ch37 Ch 38 Antibacterial Agents Penicillins and Cephalosporins I. Types of Bacteria according to their shape and the use of Gram staining A. Gram Positive If the bacteria after using Crystal violet or methalyne blue stain keep a purple stain. Examples: Staphylococcus aureus, Streptococcus pneumoniae, Group B streptococcus, and Closteridium perfingens. B. Gram Negative Bacteria- doesnt stain. Examples would be: Neisseria meningitides, Escherichia Coli, Haemophilus Influenzae. C. Antibacterials/Antimicrobial substances that inhibit bacterial growth or kill bacterial and other microorganisms including fungus viruses, protozoa. D. Antibiotic refers to the chemical produced by one kind of microorganism that inhibits the growth of or kills another. Remember that antibacterial drugs dont work alone we use other treatment modalities to assist such as natural body defenses, surgical procedures to excise infected tissue and dressing changes. They are either obtained for natural sources or manufactured. Five mechanisms of -action:

1. Inhibition of bacterial cell- wall synthesis 2. Alteration of membrane permeability 3. Inhibition of protein synthesis 4. Inhibition of the synthesis of bacterial ribonucleic acid (RNA) and Deoxyribonucleic acid (DNA) 5. Interference with the metabolism with the cell. E. Bacteriostatic verses Bactericidal drugs : 1. Bacteriostatic drugs - inhibit the growth of bacteria. Example drugs are tetracycline and sulfonamides 2. Bactericidal drugs - kill the bacteria. Example of drugs Penicillin and cephalosporin. II. Penicillins and Cephalosporins Pencillin is a natural antibacterial agent obtained from the mold genus Penicillium. Was introduced to the military in 1945 during World War II. Pencillins can be both Bactericidal and Bacteriostatic. Penicillin G is primarily bactericidal. When Penicillin G is given orally only about 1/3 of the dose is absorbed that is why it is primarily given by injection. The aqueous form has a short duration of action time and the IM is very painful. A. A Longer acting form of Penicillin is Pencillin V (V-Cillin K) although 2/3 of the oral dose is absorbed by the G.I. tract, it is a less potent than Penicillin G.Penicillin V is affective against mild to moderate infections including Anthrax. Initially penicillin was overused. It was used to treat staphylococcal infections but after a few years mutant strains of staphyloccus developed that were resistant to both forms G & V penicillin. NOT RECOMMENDED IN RENAL FAILURE. Take drug after meals. B. Board Spectrum Penicillins (Aminopenicilins)- they are not as board spectrum as was originally thought. This group of drugs is more expensive than other penicillins. T hey are effective against some gram-negative organisms like Eschericha colia, Haemophilus Influenzae, Shigella dysenteriae, Proteus mirabilis a nd Salmonella. C. Examples are- Ampicillin (Omnipen) , Amoxicillin ( Amoxil) , Bacampicillin (Spectrobid). Amocillin is the most prescribed for adults and children.
They can interfere with the effectiveness of oral contraceptives. Potassium levels can increase when taking with Penicillin G of V. Used in the treatment of lower respiratory infections, ottis media, sinusitis, skin infections & UTIs. D. Penicillnase- Resistant Penicillins (antistaphlylococcal pencillins) are used to treat penicllinase producing S. aureus. penicillin 1. dicioxacillin 2. carbenicillin 3. bicillin 4.amoxicillin 1. PCN V: po, mild-mod infection 2. PCN G: IV/IM, mod-severe infection 3.procaine PCN G: IM, decrease pain Used to treat infection. check allergies to PCN & "CEPHs" Send culture to lab Labs: BUN, creatinine. monitor VS, urine output. increase fluids. Food may decrease absorption TAKE 1HR ac & 2hr pc HAVE epinephrine available Cephalosporins In 1960s were used with clinical success however there chemical molecules had to be altered and a semi synthetic cephalosporin was developed. Active against

gram-positive and gram- negative bacteria. They are effective by inhibiting the bacterial enzyme necessary for cell wall synthesis. Lysis of the cell occurs and thus the bacterial cell dies. A. First generation Examples are Cefazolin Sodium ( Ancef, Kefzol ) B. 2nd generation Cefaclor ( Ceclor) 2nd, 3rd, and 4th Generation Cephalosporins. These drugs are bactericidal with actions similar to penicillin. It is the 3rd & 4th generations that are effective in treating sepsis and many strains of gram-negative bacilli. Examples- Aztreonam, Imipenem- cilastain. There is a 10% chance that a patient who is allergic to Penicillin will also be allergic to cephalosporins -Other Cephalosporins- Ceftazidine ,Cefepime, along with Aztreonam & Imi-Pen is effective against Pseudomonas Aeruginosa. Side Effects and Adverse Reactions GI disturbances (N/V, diarrhea), alterations In blood clotting time (bleeding potential), and when large dosages are administered Nephrotoxicity Interactions with other substances & other drugs Alcohol may cause flushing, dizziness, H/A, N/V, and muscular cramps. Drug Interactions If taking Uricosuric there will be a in the excretion of the cephalosporin drug, which will then increase the serum blood level of the drug

antifungals "zole"drugs amphotericin yeast, fungal pneumonia, ringworm, jock itch, athlete's foot AMPHOTERRIBLE: IV SLOWLY only, life threatening fungal infections LABS: liver enzymes(NEPHRtoxic)BUN, creatinine, bilirubin protect from light NO ALCOHOL be careful of thromophlebitis at IV site SE: shake & bake(fevers/chills) *****premedicate w/tylenol & benadryl*** flu/herpes (antivirals) Tamiflu take w/in 48 hrs of onset flu shot inactive nasal is live virus(live virus not for young, preggo, or immunocompromised) flu shot yearly unless ALLERGIC to EGGS of HX of GUILLIANE-BARRE IV: slow lots of H2O SE: NEPHROtoxicity, OTOtoxicity

Macrolides, Tetracyclines, Aminoglycosides and Fluoroquinolones

Macrolides , Lincosamides, and Tetracycline are primarily bacteriostatic & may be bactericidal depending upon the drug dose or the pathogen. A. Macrolides- are called Board spectrum antibiotics reflecting their large size. At l ow doses Macrolides have a bacteriostatic effect, and with a high dose they are bactericidal. They can only be administered IV, and must be given slowly to avoid pain (Phlebitis), and they are not given Intramuscular because it is too painful. Active agents against most gram- positive bacteria and moderately active against some gram- negative bacteria. Resistant strains may emerge during treatment. Used to treat mild to moderate infections of sinuses, GI tract, soft tissue, diphtheria, impetigo contagiosda, a nd sexually transmitted diseases. These drug suppress the bacterial protein synthesis.

Onset is for an oral dose is 1 hour, peak is 4 hrs. and duration is 6 hrs. The newer f orms have a longer half life and are administered less frequently 2. Examples Azithromycin (Zithromax), clarithromycin (Biaxicn) and erythromycin (E-mycin). Erythromycin {gastric acid destroys erythromycin in the stomach so acid resistance salts are added to erythromycin to dissolution in the stomach. This will allow the drug to be absorbed in the intestine. It is the drug of choice for treatment of mycoplasma pneumonia and Legionnaires disease.

erythromycin macroglides PCN SUBSTITUTE TX of respiratory infections, skin infections, babies eyes LAB: liver enzymes(AST 0-35 & ALT 4-36)send sample to lab GIVE w/full glass of H2O IV:dilute,infuse SLOWLY NEVER IM (too painful) Low dose: bacteriostatic High dose" bacteriocidal SE: HEPAtoxicity, GI disturbances
Clarithomycin- (Biaxcin) is a taken twice /day for 7 days. Azithromycin Zithromax has a longer half life and is only taken one/day for a total of 7 days. Prescribed frequently used for upper and lower respiratory infections, gonerrhea and skin infections. Remember to monitor liver enzymes (alkaline phosphatase, alanine aminotransferase, & bilirubin. Administer 1 h before or 2 hrs. after meals.Give with a full glass of water not fruit juice. Pharmocokinetics- 37% is absorbed and 51% is PB. Metabolism is t1/2 68 hrs. Excretion in bile and small amt. in urine. Pharmacodynamics Onset 1 hr. Peak 2.5 hrs. Duration- 24 hr Side Effects- GI disturbance, Hepatic toxicity. Tinnitus Adverse Reactions- Superinfections, vaginitis, urticaria, stomatitis and hearing loss. Lincosamides like erythromycin inhibit bacterial protein synthesis and have both bacteriostatic and bactericidal actions depending upon the dosage of the drug. A. Examples Clindamycin(Cleocin) widely prescribed d/t active against most grampositive organisms like Staphylococcus aureus and other anaerobic organisms. It is also absorbed better in the GI tract than lincomycin (Lincocin), and has fewer side effects than lincocin. B. Side Effects- Both can cause GI irritation, rash. C. Severe Adverse Colitis and anaphylactic shock. D. Drug interactions Both are incompatible with aminophyline, phenytoin (Dilantin), barbiturates and ampicillin.

Vancomycin treats MRSA narrow range LABS: BUN 10-20, creatinine 0.5-1.2 baseline hearing get peak and thru levels get culture before starting therapy drinks lots of H2O SE: NEPHROtoxicity, OTOtoxicity, given too fast RED MAN SYNDROME due to vasodilation
Vancomycin (Vancocin) a glycopeptides bactericidal antibiotic was used widely to treat staphylococcal infections. Vancomycin is also used against drug- resistant Staphylococcus aureus, and in cardiac surgical prophylaxis for patients whom are allergic to penicillin. It is

ineffective for treating enterococci. A. Pharmokinetics given orally to treat staphylococcal entercolitis & antibiotic associated pseudomembranous colitis d/t Clostridium difficile. When it is given orally it is not aborbed systemically & is excreted in the feces. Vancomycin given IV is effective to treat severe infections d/t MRSA, septicemia, bone, skin and lower respiratory tract. It must be diluted in 250 ml of D5 W, NS or LR. and administered at of a rate of 10mg/min, when given IV it is excreted in the urine and 30% is PB. Half life is 6 hrs. B. Pharmacodynamics inhibits the bacterial cell wall synthesis and is active against several gram-postitive microorganisms. 1. Peak is 30 minutes after the end of the infusion C. Side Effects Vancomycin may cause nephrotoxicity and ototoxicity. May also cause chills, dizziness, fever, rashes, N/V , and thrombophelbitis at the injection site. Redman Syndrome if the IV infusion is given too rapidly which is more a toxic effect rather than an allergic reaction D. Adverse Reactions Severe hypotension, tachycardia, generalized tingling, rarely cardiac arrest, eosinophilia, neutropenia, and Stevens- Johnson syndrome E. Drug Interactions Dimenhydrinate(Dramamine) if taken with vancomycin may mask ototoxicity. The risk of nephrotoxicity may be potentiated when taken with Furosemide, aminoglycosides, amphotericin B, colistin, cisplatin, and cyclosporine. Ketolides Newer classification of antibiotics structurally related to macrolides. Telithromycin (Ketek) used for adults and those older than 18 to treat acute chronic bronchitis, acute bacterial sinusitis and community acquired pneumonia. These disorders are usually caused by Strptococcus pneumonia and Haemophilis influzena. A. Pharmacokinetics- Ketek is given orally and is well absorbed from GI tract and is not affect by food intake. It is excreted in the feces and urine. It is 60-70% PB. Half life is 10 hrs. B. Pharmacodynamics Blocks protein synthesis in microorganisms. 1. Peak is 1 hr. 2. Side Effects visual disturbances, stomatitis glossitis, gastritis, N/V, abdominal distention, flatulence, oral and vaginal candidiasis, constipation, and watery stools. 3. Adverse Reactions Ketek may also lead to an exacerbation of myasthesis g gravis. 4. Drug Interactions if taken concurrently with anti-lipidemics (simvastatin, lovastatin, atorvastatin), class 1A or class antidysrhythmics. Ketek blood levels are decreased when taken with rifamin, phenytoin, carbamazepine, phenbarbital, producing a sub-therapeutic level. Tetracyclines were the first broad-spectrum antibiotics effective against gram- positive and negative bacteria, mycobacteria, rickettsiae, spirochetes, and chlamydiae. Tetracyclines act by inhibiting bacterial protein synthesis and have a bacteriostatic effect. They are not effective against Staphylococcus aureus(except for the newer forms of tetracycline),Pseudomonas, or Proteus. Tetracycline in combination with metronidazole and bismuth subsalicylate is useful in treating Helicobacter pylori(bacterium in the stomach that can cause peptic ulcer).It can be given orally, intramuscular, or intravenously. IM is very

painful and is seldom used. Newer oral forms are : Doxycycline minocycline and methacycline these preparations should not be taken with aluminum and magnesium antacids, milk products containing calcium, or iron- containing drugs d/t substances binding with tetracycline and prevent absorption.

Tetracycline DOXYCYCLINE BROAD spectrum, bacteriostatic po/IV, NEVER IM(too painful) txs acne & tick-born illness LABS: BUN, creatinine, culture before starting therapy. TAKE on EMPTY STOMACH NO MILK(admin 1 hr ac & 2hr pc) NO ANTACIDS NO PREGGOS because pills less effective SE: photosensitivity, tertogenic, gray teeth, NEPHROtoxicity Doxycycline & Minocycline- there absorption is improved with food ingestion. A. Side Effects GI disturbances such as N/V, diarrhea. Photosensitivity may occur especially when taking Demclocycline (Declomycin).Pregnant women should not take tetracycline during the 1st trimester d/t possible teratogenic effects. Women in their last trimester and children older than 8 yrs. should not take tetracycline d/t irreversibly discoloration of the permanent teeth. Minocycline(Minocin)can cause damage to the vestibular part of the inner ear which leads to difficulty maintaining balance.
B. Adverse Reactions Nephrotoxicity results when higher doses of tetracycline have been given. It can also disrupt microflora in the body and lead to Superinfection. C. Drug Interactions Antacids (Maalox and others) and iron-containing drugs can prevent absorption of tetracycline from the GI tract. Milk and other drugs high in calcium can do the same, so to avoid decrease absorption of tetracycline while those drugs they should be taken 2 hrs,apart from the tetracycline. The desired effect of oral contraceptives can be lessened when taking with tetracyclines. Administering tetracycline with an aminoglycoside may increase the risk of nephrotoxicity. tetracycline NO DAIRY!!!! NO PREGGOS!!!!! can cause grey teeth so NO KIDS!!! Aminoglycosides They act by inhibiting bacterial protein synthesis. They are used against gram- negative bacteria such as E. coli, Proteus spp , and Pseudomonas. Streptomycin was the 1st aminoglycoside available for clinical use to treat tuberculosis. D/t its ototoxicity it is infrequently used today. It is however the drug of choice for tularemia & bubonic pneumonic forms of the plague. Aminoglycosides are used for serious infections. They cannot be absorbed from GI tract and cannot cross into the cerebrospinal fluid. They do cross the blood brain barrier in children but not in adults. They are primarily given IV or IM. Neomycin, or paramomycin are 2 types of a minoglycoside that can be given orally . Neomycin is given for a pre-op bowel antiseptic and paramomycin is useful for treating intestinal amebiasis and tapeworm infections. Tobramycin, Amikacin , and Netilmicin are newer aminoglycoside. Gentamycin(Garamycin) is currently used to treat Pseudomonas Aeruginosa A. Pharmacokinetics of Gentamycin has a short half life and the drug can be given 3-4 times/day. It is primarily excreted unchanged in the urine. Pharmacodynamics- Inhibit bacterial protein synthesis and have a bactericidal effect. 1. Onset- is rapid or immediate

same

2. Peak is 1 hr 3. Duration 6-8 hrs. C. Side Effects/ Adverse Reactions Ototoxicity and nephrotoxicity. Drug Interactions- When aminoglycoside are given with penicillins the desired effects are greatly decreased. Actions of warfarin can be increased if taken at the time as an aminoglycoside.

aminoglycosides "mycin" gentamycin neomycin sreptomycin gram-for serious infections IM>IV, except neomycin (po) neomycin decreases ammonia level. assess VS,urine output. MAY DECREASE K+ & Mg+ renal & hearing baseline. check for neurotoxicity & ototoxicity LABS: BUN, creatinine. IV dilute & infuse 30-60 mins. culture before & after starting therapy monitor I/O's, hearing, labs. PUSH FLUIDS peak &thru levels(narrow TI) SE: NEPHROtoxicity, OTOtoxicity
Fluoroquinolones(Quinolones) - The mechanism of action is to interfere with the enzyme DNA gyrase, which is needed to synthesize bacterial DNA. Their antibacterial spectrum includes both gram- positive & negative organisms. They are bactericidal. The fluoroquinolones that is effective against some gram- positive organisms such as Haemophilus influenza, Proteus aeruginosa, Salmonella and Shigella. Effective for treatment of urinary tract infections; bronchitis; pneumonia; gastroenteritis; and gonorrhea. Examples: Ciprofloxacin (Cipro)and Norfloxacin (Noroxin) are synthetic antibacterials related to nalidixic acid and are broad spectrum on both gram- positive and negative organisms. Both are indicated for urinary tract infections; lower respiratory infections; skin; soft tissue; and bone and joint infections. In the past few years the number of fluoroquinolones has increased. Levofloxacin (Levaquin) used for community pneumonia, chronic bronchitis, acute sinusitis. Pharmacokinetics approximately 70% of Levaquin is absorbed from the GI tract. It has a low PB effect. Moderately short half life of 6.5-7.5 hrs. More than 75% is excreted unchanged in the urine. Pharmacodynamics- This drug has a high tissue distribution. If possible should be taken before meals, d/t food slowing down absorption rate. Antiacids also decrease absorption. Levaquin increases the effect of oral hypoglycemic, theophylline and c affeine. 1. Onset 30 minutes to 1hr 2. Peak 1-2 hrs. 3. Duration- is unknown

fluoroquinolones ciprofloxacin levofloxacin gatifloxacin BROAD spectrum. interfers w/the enzyme DNA gyrase. treats anthrax, UTI, resp. infection, skin infection. LABS: BUN, creatinine. increase fluid intake NO PREGGOS monitor I/O's antacid & iron lower absorption SE: nausea, vomiting, diarrhea ,ARCHILLES tendon rupture, tinnitus antimalarials Aralen prophylaxis(before,during,after trip) S & SX: fevers, chills, sweats. assess hearing & visual changes. take W/FOOD Avoid alcohol caused by parasitic protozoal destroys RBC,

impairs O@ delivery SE"GI upset, cranial nerve 8(hearing) involvement, renal impairment antitubicular Isoniazid (INH) give if they have been exposed treats TB prophylaxis AFB isolation negative pressure prevent peripheral neuropathyw/vitamin B6 (pyridoxine)(INH) collect early am sputum for acid fast bacillus X3 S & sx: night sweats, fever, productive cough give 1h ac or 2h pc DOTS tx: directly observed tx eye exams NO ANTACIDS!!! SE: HEPAtoxic, jaundice antitubercular Rifampin (if active TB) treats active TB collect early am sputum for acid fast bacillus X3 S & sx: night sweats, fever, productive cough give 1h ac or 2h pc DOTS tx: directly observed tx SE: brown rust discolor

Ch 42-46 Antiinflammatory and Antigout Drugs

Inflammation -is our bodys normal protective response to neutralize and destroy harmful agents at the site of tissue injury. Infection- is caused by the presence of microorganisms and results in inflammation, but NOT all inflammations are infections - Five Cardinal signs of Inflammation - because cardinals are red! - Erythema - Redness occurs in the 1st phase of inflammation. Blood accumulates to the injury site d/t ( kinins, prostaglandins,& histamines) - Edema - swelling 2nd phase of inflammation. Plasma leaks into interstitial tissue at injury. Kinins dilate arterioles cap. Permeability. - Heat - can be caused by the inflammation at the site d/t blood accumulation and may result from pyrogens - Pain- Caused by the chemical mediators that were released by injured tissues and the tissue swelling - Loss of Function Loss of function accurse d/t fluid accumulations and d/t pain which decrease mobility. Chemical Mediator that are released during the Inflammatory processA. Prostaglandins- have many effects vasodilation, relaxation of smooth muscle, capillary permeability and sensitization of nerve cells to pain. B. Cyclooxygenase (COX) - enzyme responsible for converting arachidonic acid into prostaglandins & their products. 2 forms of the cyclooxgenase COX-1 - protects the stomach lining and regulates blood platelet, promoting clotting COX-2 - triggers the inflammation and pain responses. Anti-Inflammatory Agents Group of drugs that inhibit the synthesis of prostaglandin they are called prostaglandin inhibitors, but are most commonly called anti-inflammatory agents. They have potent antiinflammatory effects that mimic the corticosteroids they are also known as NSAIDS (Nonsteriodal Anti-Inflammatory Drugs. Some of the newer NSAIDS block only the COX-2.

anti-gout Allopurinol low serum uric acid levels, prevents attacks. assess uric acid levels, CBC, uric acid foods: wine, alcohol, organ meats, sardines, salmon, gravy. check I/O's, increase fluid, take

AFTER MEALS, yearly eye exams. "disease of kings""unwalkable disease" inflammation condition, attacks joints & tendons. Caused by excess uric acid . SE: pruritus, metallic taste, GI upset/bleed, malaise acetaminophen: Tylenol, Excedrin, goody's, Midol fever, pain, HA monitor HEPAtoxicity AST 0-35 ALT 4-36, pain check for jaundice and bleeding ANTIDOTE: mucomyst causes little to no GI disturbances
Acetylsalicylic Acid (Aspirin) was developed in 1899 by Adolph Bayer. It is a prostaglandin inhibitor in the inflammatory process. It is also an Anti Platelet. Remember that ASA should not be used with other NSAIDS. Common symptom of sensitivity to Salicylate is Tinnitus (ringing in the ears) ,vertigo, bronchospasm. Many foods have salicylates in them such as wine, prunes, curry, and licorice. Para- Chlorbenzioc Acid- Used to treat Rheumatoid ,Gout and Osteo- Arthritis. Potent prostaglandin inhibitor, 90% protein bound and displaces other protein bound drugs drug toxicity. Half life is 4-11hrs. 1. Examples Indomethacin (Indocin) which is very irritating to the stomach and should be taken with food. Sulindac (Clinoril), Tolmetin (Tolectin) these drugs produce less severe reactions then Indocin and may cause retention of Na and H2O Phenlacetic Acid Derivatives effects are similar to aspirin, but minimal anti-pyretic properties. Used for same arthritic conditions as para-chlorbenzoic acid but also for anklosing spondylitis. - Examples Diclofenac sodium (Voltaren) and Ketorolac (Toradol). Toradol was the first injectable NSAID that has high analgesic properties which are = to that of opiods. Intramuscular dose is 30-60mg q 6 hrs.

NSAID aspirin (ASA) falls under multiple classes Analgesic antipyretic, antiplatelet, anti-inflammatory, menstrual pain. Check for ASA allergies. assess hx for GI upset, bleeding & liver disease. TAKE with FOOD or FULL glass of WATER. admin PPI to reduce risk of ulcer. SE: no PREGGOS LAST TRImester, n alcohol, don't take w/other NSAIDS, kids with flu like sx cant take (reye's syndrome) SE: GI upset, bleeding, renal failure, TINNITUS
Fenarnates and Oxicams are the last two classification of 1st generation of NSAIDs. COX2 inhibitor is Celecoxib (Celebrax) only one true . Remember biggest Cautious use listed was Heart Failure and Bleeding tendencies.

(2nd generation NSAID) cox 2 inhibitor Celebrex TX of osteoarthritis & rheumatoid arthritis, menstrual discomfort. LONG TERM use. assess for HX of RENAL or HEPATIC dysfunction, HYPERtension, fluid retention, heart failure, infection, GI bleeding or ulceration, concurrent anticoagulant therapy, steroids, or alcohol use. INCREASE FLUID intake. monitor RENAL function. SE: HA, sinnusitis, flatulence, peripheral edema, GI upset/bleed Cox 2 inhibitor Celebrex used for osteoarthritis SE:GI upset

NSAID Toradol analgesic. INTRAOCULAR anti-inflammatory. monitor RENAL/HEPATIC function. observe client for signs of bleeding. SHORT term use for pain. OPTHALMIC-relieve itching caused by allergic conjunctivitis. SE: HA, nausea, peptic ulcer, hepatic reaction, nephrotoxicity in pts. w/preexisting renal impairment
Propionic Acid New group of NSAIDs but are stronger than ASA but have less GI irritation. Examples Ibuprofen (Motrin Advil), Fenoprofen Calcium (Nalfon), Naproxen (Naprosyn), Ketoprofen (Orudis), Flurbiprofen (Ansaid) and Oxaprozin ( Daypro). Corticosteriods Have a long half life of > 24 hrs. When drugs are D/C the dose be tapered over a period of 5-10 days before it is just stopped. Examples Prednsone, Prednisolone and Dexamethazone. should

Disease Modifying Antirheumatic Drugs these therapies include such elements as Immunosuppressive Agents, Immunodulators , & Antimalaries. Antigout Drug - Gout inflammatory condition that affects the joints, tendons, and other tissues. Characterized by a buildup of urates (uric acid salts) uric acid levels(hypouricemia) d/t kidneys being unable to excrete. Also uric acid my buildup in the kidneys causing uric acid calculi. When patient are on anti-gout medication make sure that fluid intake is .Patients should be instructed to avoid alcohol. They should also take Tylenol for discomfort instead of aspirin d/t aspirin would the acid levels even more. Examples of anti-gout medications are Uric acid inhibitors like Allopurinol (Zyloprin) . Uricosurics increase the rate of uric acid excretion by inhibiting its reabsorption. They are used for the chronic condition not an acute attack. Potential side effects flushed skin, sore gums, and headache. Also might cause a metallic taste. Instruct patients to avoid alcohol and caffeine because they can uric acid levels. Examples - Probenecid (Benemid)- this drug may cause gastric irritation and when this occurs should be taken with food. Sulfinpyrazone ( Anturane)- is even more potent the Benemid and should be taken with food or with and antacid to prevent gastric irritation.

Ch 22 Heart failure drugs Ch 23Antidysrhythmic drugs Ch 24Antianginal drugs

Cardiac Glycosides They are a group of drugs that inhibit the sodium- potassium pump, resulting in in intracellular Na Ca which causes cardiac muscle fibers to contract more efficiently. Three effects on the heart muscle are : 1. Positive Inotropic action- ( on mycocardial contraction& stroke volume). 2. Negative Chronotropic action- ( the heart rate)

3. Negative Dromotrophic action- (conduction of the heart cell) The in myocardial contractility increases cardiac, peripheral and kidney function by CO, preload, improving blood flow to the periphery and kidneys, edema, and increasing fluid excretion. Glycosides Used for the Treatment - Atrial Fibrillation and Atrial Flutter with rapid Ventricular response with rates 200-300 beats/min. REMEMBER DIGOXIN DOES NOT CONVERT A- FIBRILLATION TO NORMAL SINUS RYTHYM Drugs used for Treatment of Heart FailureFirst drugs of choice is Inotropic medication like Dopamine and Dobutamin, Phosphodiaesterase inhibitors like ( Inamrinone, & Milrinone -Primacor), Diuretics, Beta blockers, ACE inhibitors, Angiotension Receptor Blockers(ARBs), Calcium Channel Blockers and Vasodilators. Lab Values to consider to confirm diagnosis of Heart Failure in patients with other Lung Pathophysiological disorder-ANP- Atrial Natriuretic Hormone Peptide 20- 77 ng/l (An elevation may confirm Heart Failure. It is secreted from the atria of the heart and acts as an antagonist to the renin and aldersterone. It is released during the expansion to the atrium, produces vasodilation , and glomerular filtration rate. - BNP- Brain Natruiretic Peptide- Desired level < 100 pg/l. A positive result is recorded as > 100 pg/l and aides in diagnosing Heart failure. It is a more sensitive test than ANP . Today there is an emergency bedside test available for measuring BNP.

Digoxin pos. inotrop neg. chronotope Increases force of contraction and decreases HR. for heart failure and dysrhthmias. narrow therapeutic(0.5-2)hold for Bp less than 60.monitor for BRADYCARDIA, halos around lights. HyPOKalemia cause more risk for toxicity cause as potassium drops the cardiac muscles sensitivity increases. RENAL impairment because KIDNEYS cant excrete digoxin. watch BUN/CREAT antidote: digibind. EAT high POTASSIUM!!
Other drugs used to treat Heart FailureDigoxin (Lanoxin) - Pharmacokinetics - Absorption is 90-100% in the capsule form (remember that because of the longer half life that the drug accumulation should be monitored very carefully). Excretion is 70% in the urine and 30 % by liver metabolism. -Pharmacodynamics used in treatment of heart failure. They myocardial contraction and cardiac output and improves circulation through the Atrial Ventricular node the heart rate . - Digitalis Toxicity Signs & Symptoms Anorexia, diarrhea, N/V, H/A, Bradycardia, PVCs, blurred vision, (white & green halos), confusion, and Delirium. Digitalis toxicity can lead to first degree hear t block then to 2nd degree AV block and finally to a third or complete heart block. The antidote for Digitalis Toxicity is (Ovine, Digibind) this agent binds with digoxin to form complex

molecules that can be excreted in the urine. -Herb Interactions Ginseng may falsely digoxin levels. St. Johnss wart- absorption of digoxin. Psyllium (Metamucil) digoxin absorption Hawthorn - may the effect of digoxin Licorice- promotes K+ loss digoxin toxicity. Other Drugs used to Treat Heart Failure- Vasodilators, Angiotension Converting Enzyme Inhibitors, Angiotension II Receptor Antagonist Blockers, Diuretics, Aldactone, & some Beta Aderenergic Blockers. Vasodilators- venous blood return which decreases cardiac filling, ventricular stretching (pre-load) and O2 demand on the heart. Arteriolar dilators act in 3 ways - Reduce cardiac after load which cardiac output. - Dilate the arterioles of the kidneys which improves renal profusion and fluid loss - prefusion to the skeletal muscle ACE inhibitors - usually prescribed for Heart failure to dilate venules and arterioles improving renal blood flow(profusion) and blood fluid volume also moderately Aldesterone which can K+ levels.

Ace inhibitors "prils" used to treat HTN. doesnt let angiotensin 1 convert to angiogenesis 2.lowers BP with no effect on HR. used with DM and HTN. prevents stroke, MI due to inflammation. used for renal protection=lowers pressure in glomerus; protects the kidneys. Can lead to HYPERKalemia. Angiotensin 2 Bad cause it increases inflammation, clots and resistant to insulin. SE=cough, HYPERKalemia. Assess: BP, urine protein, BUN/CREAT, CBC,K, and Na levels. COUGH, HYPOtension, HYPERKalemia, may lose taste for food. NOT for RENAL
Angiotension II Receptor Blockers- Valsartan(Doivan) and Cardesartan(Atacand) have been approved for Heart Failure for those clients whom cant tolerate ACE inhibitors. Diuretics First line of drugs for Heart Failure when you are trying to fluid volume used with Digoxin or other agents. -Spirolactone (Aldactone) K+ sparing , used for moderate to severe Heart Failure. to blocks the production of Aldesterone. (Normally with Heart Failure the Aldesterone production goes up Na and Water retention K+ and Magnesium loss ( both electrolytes are need for the hearts contracts. Beta Blockers usually contraindicated for clients with Heart Failure. Reduces contractility - Carvedilol- (Coreg) and Metopropolol( Toprolol)- have been shown to improve cardiac performance. Beta Blockers "Inderal (non-selective) all others selective. decreases contractibility in heart, lowers renin release in KIDNEYS, and sympathetic output. For HTN, angina, MI, dysrhthmias. SE=BRADYcardia, hyPOtension, bronch constriction, lowers blood sugar. Hold for BP less than 60 or systolic less than 90. Inderal can

decrease test anxiety

Nesiritide (Natrecor)- an atrial Natuiretic Peptide hormone that inhibits Anti- Diuretic hormone by Na loss (causes vasodilation, natriuresis, And diuresis. Bi- Dilators combination of Hydralizine (which B/P) and Isosorbide dinatrate ( a dilator to relieve heart pain) in 2005 FDA approved it for the treatment of Heart Failure especially in African Americans(who are 2 times more likely to have Heart Failure than are Caucasians. Anti Anginal Drugs- Acute Cardiac pain caused by inadequate blood flow to the myocardium due to plaque, occlusion within or spasms of coronary arteries. There are three types: -Stable (Classic) occurs with stress or exertion - Unstable (Pre-Infarction) occurs frequently over the course of a day with proseverity. -Variant (Printz Metal or Vasospasic)- occurs during rest often wakes pt. from a sleep. Non- Pharmacological Measures- Avoid eating a heavy meals, smoking, extremes in weather changes, strenuous exercise , emotional upsets, proper nutrition and rest, moderate exercise. Pharmacological Agents- Anti- Anginals work one of 2 ways : Either it O2 supply or by O2 demand by the myocardium. Three types of medications are: 1. Nitrates 2. Bate- Blockers 3. Calcium Channel Blockers Nitrates- major systemic effect is they venous tone, which workload of the heart and promotes vasodilatation. Beta Adrenergic & Calcium Channel Blockers the workload of the heart by O2 demands. Nitrates and Calcium blockers are helpful in the treatment of Variant Angina because they actively preload and afterload both of which O2 demand. - Sublingual NTG 0.4 mg or 1/150 gr can be repeated every 5 minutes for a total of 3 doses. Effect last for 10 minutes. Must be protected from light and heat. - Isosorbide Dinatrate ( Isordil Sorbtrate)- available sublingual, chewable tablets, immediate release tablets, and sustained released. -Nitroglycerine ( Nitrostat, Nitro-Bid, Transderm Nitro Patch, Nitrogard SR used to control angina pectoris (angina pain). - Pharmacokinetics: Approximately 40-50% GI tract inactivated by the liver. SL > 75% absorbed rapidly directly into the internal Jugular Vein Right Atrium. Topical Transderm Nitro Patch- slow absorption by the skin acts on the smooth muscle, blood vessel, causing relaxation & dilatation cardiac preload and after load( Peripheral vascular resistance) myocardial O2 demand. - Pharmacodynamics- SL- Onset- 1- 3 minutes, Peak- 4 min. Duration- 2030 min Slow Released Onset 20-45 min. Duration- 3-8 hrs. Ointment Onset 20 -60 min Peak 1-2 hrs. Duration 6-8hrs. Patch -

Onset 30- 60 min Peak 1-2 hrs. Duration20-24hrs. I.V. - Onset 1-3 min. Duration 3-5 min. - Side Effects nausea, vomiting, H/A, dizziness, syncope, weakness, flush, confusion, pallor, rash, dry mouth. d. Adverse Reactions: Hypotension, reflex tachycardia, paradoxical bradycardia. e. Drug-Lab-Food Interactions effect with alcohol, beta-blockers, calcium channel blockers, antihypertensives, effects of heparin. Beta Adrenergic Blockers Beta I and Beta II the effects of the Sympathetic nervous Systems by blocking catecholamines Epinepherine and Norepinepherine which heart rate and blood pressure. Used as an anti-anginal, anti-dysrhythmic, and antihypertensive. Patients should be told that they should NOT abruptly stop these medications. - Beta1- Atenolol ( Tenorium) - It can be used with asthmatic patients. -Metoprolol( Lopressor)- Beta1 . High dose can effect Beta2 Bronchoconstriction -Beta1 and Beta2 - used to treat Angina Pectoris and hypertension - Nadolol (Corgard) - Propanolol (Inderal) . Risk for Bronchospasms Calium Channel Blockers - myocardial contractions O2 demand by myocardial tissue. Relax coronary artery spasms and peripheral arterioles, cardiac oxygen demand. Amilodipine (Norvasc) - Angina and Hypertension 1. Diltiazem ( Cardizem) - Used for treatment of Angina Pectoris, its hypotensive effect is not as severe as with procardia. Kidney function should be monitored, 2. Nifedipine ( Procardia) - . It is used for to treat angina pectoris and hypertension. Suppresses contraction of cardiac and vascular smooth muscle. Increases heart rate and cardiac output. Decreases blood pressure. Three of the Calcium Channel Blockers are used for the long term treatment of Angina Verapamil( Calan), Nifedipine (Procardia), and Diltiazem (Cardizem). Procardia is the most potent. Side Effects H/A, hypotension ( more common with procardia) and less common with Diltiazem. calcium channel blockers Calan, ProCardia, Cardizem lowers myocardial contraction and eases workload, lowers HR and BP, raises blood flow to heart, lowers peripheral vasorestiction for HTN, angina, A-fib, migraines SE=HYPOtension, HA, "blah" feeling....monitor hepatic and renal function, assess BP and HR Antidysrhythmia - A dysrhythmia is any deviation from a normal rate or pattern of a heartbeat. 1. Dysrhythmia- disturbance of a heart rhythm. 2. Arrhythmia- absence of a heart rhythm 3. Aterial Dysrhythmia- prevents ventricular filling and. 4. Arrhythmia- absence of a heart rhythm 5. Aterial Dysrhythmia- prevents ventricular filling and cardiac output by 1/3 6. Ventricular Dysrhythmia- are life threatening because of ineffective filling of the ventricle resulting in or absence of cardiac output.

7. Cardiac Dysrhythmias commonly occur after a M.I.(myocardial infarct) or hypoxia or hypercapnia (level of CO2 in the blood) , thyroid disease, C.A.D., Cardiac Surgery, Excessive catecholamines, or electrolyte imbalances. 8. Action Potential- Remember when Na+ and Ca+ enter the mycocardial cells muscle contraction and depolarization occurs. Anti-dysrhythmia drugs- there are four class of anti-arrhythmic drug which effect the different phases of the action potential. Class I: Sodium Chanel Blockers: -Slow condition which prolongs Repolarization (Atrial and Ventricular such as PAT- Paroxysmal Atrial Tachycardia and SVT Supra Ventricular Tachycardia) -Slow conduction that shortens Repolarization(Acute Ventricular Dysrhythmias) -Prolong condition with little effect on Repolarization (Life threatening Ventricular dysrhythmias). Class II: Beta Blockers: Reduce Ca+ entry, conduction velocity ,automaticity and recovery time (refractory period) Used to treat (Atrial flutter & Fibrillation, tachydysrhythmias and Ventricular and Supraventricular dysryhthmias). Class II Beta-Adrenergic Blockers- (more frequently used prescription for dysrhythmias than Na+ channel blockers Acetbutolol (Sectral)-Beta1 blocker - Pharmocokinetics- Well absorbed from the GI tract. via -Metabolized in Liver to active metabolites- 50-60% is eliminated in bile feces. 30-40 is excreted in urine. Pregnancy class is B. Protein Bound: UK . -Metabolism: t : 3-4 hrs. Metabolites: 8-13 hrs. -Pharmocodynamics: Ventricular dysrhythmia: PO: Onset: 1 hr. -Peak: 4-6 hrs. -Duration: 10 hrs. For treatment of HTN duration = 20-24 hrs. Class III: Drugs that prolong Repolarization: Prolong repolarization during ventricular dysrhythmias, and prolong action potential duration. Used to treat (Life threatening Atrial & Ventricular dysrhythmias resistant to other drugs). Class IV: Calcium Channel Blockers: Block influx of Ca+, Slow conduction velocity, myocardial contractility (Negative Inotropic), and refraction in the AV node. Used to treat (Supraventricular tachdysrhythmias, prevention of Paroxysmal supraventricular tachycardia PSVT). Examples: - Na+ Channel Blockers: Class IA a. Napamide (Norpace) Adult dose PO: 100-200mg every 6 hrs. or if CR is used then PO 300mg every 12 hrs. b. Procainamide (Procanbid or Pronestyl)- Adult PO 250-500mg q 3-4

hrs., or if SR is used dose is 250mg 1 Gm. q 6 or q 12 hrs. -Na+ Class IB : a. Lidocaine (Xylocaine)- USE cautiously with patients who have Liver Failure or an AV Block. Given I.V. Bolus dose: 50-100mg over 23min.: then Continuous infusion at dose 20-50mcg/kg/min. b. Mexiletine (Mexitil)- Adult dose PO 200-400mg q 8hrs. c. Tocainide (Tonocard)- Adult loading dose is 600mg then 400mg q 8hrs. with a maximum dose of 2.4 Gm/day. - Na+ Class IC : -Flecainide (Tambor) Adult PO initial dose 50-100mg q 12hrs, dose by 50mg q 12hrs every 4 days; Maintenance dose of 150mg q 12hrs. Maximum dose of 300mg/day. Propafenone (Rythmol) Adult PO dose 150-300mg q 8hrs. Maximum dose is 900mg /day.

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-Therapuetic : to help in treatment of recurrent stable ventricular dsyrhythmias. - Side Effects: Dizziness, H/A , B//P, diaphoresis, fatigue, constipation, contraindicated in 2 or 3rd degree heart blocks, and severe bradycardia, severe HF, or in cardiogenic shock. Adverse Reactions: Palpitations with abrupt withdrawal . Life Threatening: agranulocytosis, bronchospasm with high doses. Teach patients that they should avoid alcohol, smoking and caffeine.

Propanolol ( Inderal Beta1& 2 Blockers- . , IV bolus, Used for treatment of Ventricular dysrhythmia, angina, and hypertension. Sotalol (Betapace) Beta1&2 Blockers - Adult PO 80 mg B.I.D. with a Maximum dose of 240mg-320mg/day 1. Pharmocokinetics- Well absorbed from the GI tract. 2. Metabolized in Liver to active metabolites- 50-60% is eliminated in bile via feces. 30-40 is excreted in urine. Pregnancy class is B. 5. Class III- Drugs that prolong Repolarizationa. Adenosine (Adenocard)- Adult IV initial dose is 6mg rapid bolus May repeat the dose at 12 mg IV x 2 more doses. b. Amiodarone (Cordarone) Adult loading dose is 400mg-1600mg/day. Be-aware of the photosensitivity it causes. c. Bretylium Tosylate (Bretylol)- . d. Sotalol (Betapace)- Adult PO dose is same as Class II . 6. Calcium Channel Blockers- Contraindicated in 2nd & 3rd degree heart blocks a. Verapamil (Calan Isoptin)- Adult dose 240-480 mg/day in 3 to 4 divided doses. IV 5- 10 mg IV push. b. Diltiazem (Cardizem)- 7. Other

a. Phenytoin (Dilantin)-Adult IV 100mg q 5-10 min until dysrhythmia ceases. Maximum dose 1000mg. Used for digitalis induced dysrhythmia. b. Digoxin (Lanoxin) - Adult IV loading dose 0.6-1mg/d in 24hrs.

"statin" meds given for high cholesterol change diet exercise REPORT CRAMPS TO DR LABS: AST/ALT 0-35,4-36 give at NITE except LIPITOR IN MORNING
Diuretics- Two main purposes 1. Blood Pressure;& 2. Edema (peripheral/pulmonary). Diuretics work by inhibiting Na+ and H2O re-absorption from the kidneys in the tubules thus promoting their loss through excretion in the form of urine. Five Categories of Diuretics: 1. * Thiazide and Thiazide like 2. * Loop or high ceiling diuretics 3. Osmotic 4. Carbonic anhydrase inhibitor 5. * Potassium sparing (* Most frequently prescribed for HTN, edema associated with Heart failure) 6. Combination Diuretics- (Both K+ sparing and K+ wasting) used for the treatment of HTN Thiazide- Diuretics used primarily in patients with normal renal functions. Thiazide drugs cause not only loss of Na+, K+, and magnesium they also cause calcium reabsorption, which may lead to Hypercalcemia, another consideration that it cause glucose intolerance or possible Hyperglycemia so it should be used with caution in patients with diabetes mellitus. Drug -Lab/Food Interactions: Drugs: digitalis toxicity with digitalis and hypokalemia; K+ loss with steroids; antidiabetic effect; thiazide effect with cholestramine and colestipol. Lab: serum calcium, glucose, uric acid, serum potassium, sodium & magnesium. Pharmacokinetics- Readily absorbed from the GI tract 1. 65% Protein bound 2. Metabolism: t = 6-15 hrs. 3. Excretion in the urine Pharmacodynamics- PO Onset : 2 hr 1. Peak: 3-6 hrs 2. Duration: 6- 12 hrs 3. Therapeutic Effects: to urine output, to treat: HTN, edema from HF, hepatic cirrhosis, renal dysfunction. Mode of action to Na+, K+, and H2O excretion and preload and cardiac output. 4. Side Effects: dizziness, vertigo, weakness, N/V, diarrhea, hyperglycemia, constipation, rash, and photosensitivity. 5. Adverse Reaction: Severe dehydration, hypotension, severe hypokalemia,

uremia, aplastic anemia, hemolytic anemia, thrombocytopenia,& agranulocytosis. 2. Loop (High Ceiling) Diuretics: act in the thick ascending Loop of Henle to inhibit chloride transport of Na+ into the circulation. They inhibit passive re-absorption of Na+ which leads to loss of Na+ , water, K+, Ca+, Mg+ . They can also effect blood sugar levels and uric acid levels. These groups of drugs are extremely potent causing a marked electrolyte and water depletion. Less effective as anti hypertensive agents than the Thiazides. They can renal blood flow up to 40%. Frequently prescribed when pt.s creatinine clearance is < 30ml/min. & for end stage renal disease. This group of diuretics cause Ca+ excretion where as the Thiazides inhibit Ca+ loss. Example: Furosemide (Lasix) Both Lasix and Bumex are sulfonamide derivatives for patients who are allergic to Sulfa (use Ethancrynic Acid) Lasix should never be prescribed with another loop diuretic. It should be administered in the AM when taken orally or administered IV when the clients condition warrants immediate removal of body fluid. Pharmacokinetics: PO readily absorbed from the GI tract. . 3. Excretion: In urine, some in feces: crosses the placenta. 4. Drug-Lab/Food Interactions : Drug- orthostatic hypotension with alcohol; ototoxicity with aminoglycosides; bleeding with anticoagulants; K+ loss with steroids; digitalis toxicity with digoxin and hypokalemia; lithium toxicity;amphotericin B ototoxicity and nephrotoxicity. Side Effects: dizziness, electrolyte imbalances, vertigo, cramping, rash, headache, weakness, ECG changes, blurred vision, photosensitivity. Adverse Reactions: Severe dehydration; marked hypotension. e. Life threatening: Renal failure, thrombocytopenia, and agranulocytosis. Transient deafness. Prolonged use could cause Thiamine deficiency. f. Aloe K+ level especially when taken with K+ wasting diuretics and licorice can K+ loss. Osmotic Diuretics: osmolality & Na+ re-absorption in proximal tubules and in Loop of Henle. This group of drugs are used to prevent kidney failure, Intracranial pressure, Intraocular pressure (glaucoma). Mannitol potent osmotic K+ wasting diuretic frequently used in Emergency situations. It can also be used with Chemotherapy drugs Crisplatin and Caboplatin to induce diuresis common side effect of these drugs fluid retention). Diuresis with Mannitol occurs in 1-3 hrs. for IV route. Side Effects: Fluid and Electrolyte Imbalances, pulmonary edema from rapid fluid shift, N/V, tachycardia, acidosis, crystallization of Mannitol may occur in the vial due to exposure to lower temperatures. Vial may be warmed to dissolve the crystals. CRYSTALS MUST BE DISOLVED BEFORE DRUG CAN BE GIVEN IV. MUST BE GIVEN WITH EXTREME CAUTION in Patients with Heart Disease & Heart Failure Osmotic diuretic Mannitol increases osmotic pressure, prevents water reabsorption; raises Na and Cl excretion. For:oliguria, edema, raises intracranial pressure-cerebral edema, raisesintraocular

pressure(glaucoma) . Potassium WASTER! Used in ICU/trauma setting. Assess serum osmality. SE; dry mouth, cellular dehydration, fluid and electrolyte imbalance, pulmonary edema, circulatory overload. Oliguria, Stops water, Mannitol, Output of urine(monitor), Tissue dehydration, Increased urinating, Circulatory overload
Carbonic Anhydrase Inhibitors: Acetazolamide, Dichlorphenamide, Ethoxzolamide, Methazolamide block the action of the enzyme carbonic anhydrase (needed to maintain acid/base). Inhibition of this enzyme causes Na+, K+, HCO3 excretion. These groups of drugs are used to intraocular pressure in patients with open angle (chronic) glaucoma. Other uses are for diuresis, treatment of Epilepsy, and treatment of high altitude or acute mountain sickness. Side Effects: Acetazolamide can cause fluid and electrolyte imbalance, metabolic acidosis, N/V, anorexia, confusion, orthostatic hypotension, hemolytic anemia,& renal calculi. Potassium Sparing Diuretics: Weaker drugs than the Thiazides and Loop Diuretics( daily K+ supplements are not used when patients is taking K+ sparing diuretics). Monitor : K+ levels if > 5.3 Meq/L while on these drugs, stop drugs and restrict diet of foods K+. Area of action is in the collecting ducts and distal tubules to promote Na+ and H2O excretion and K+ retention. Spironolactone ( Aldactone)- An Aldosterone antagonist. First K+ sparing diuretic. Remember Aldosterone is a mineralocorticoid secreted by Adrenal Cortex. Other examples are : Amiloride(Midamor), Triamterene(Dyrenium) Eplerenone(Inspra). They are used in treatment of edema caused by HF or cirrhosis of the liver.None of the K+ sparing drugs should be taken with ACE inhibitors & Angio II Recptor Blockers (ARBs) because they also can K+ levels. Side Effects- K+ especially with patient with poor renal function. Urine output should be @ least 600ml/day. GI disturbances like N/V, diarrhea, numbness & tingling of hands and feet. Triameterene ( Dyrenium)- Adult dose for edema 100mg/day in 2 divided doses p.c., not to exceed 300mg/day. Contraindications severe kidney or hepatic disease severe K+. Use with Caution : In patients with renal ,hepatic dysfunction and those who have diabetes mellitus. Pharmacokinetics: PO rapidly absorbed from GI tract 1. Distribution : 67 % Protein Bound 2. Metabolism: t = 1.5 2.5 hrs 3. Excretion: in urine; mostly as metabolites and bile Pharmacodynamics: PO Onset : 2-4 hr 1. Peak: 6-8 hrs 2. Duration: 12-16 hrs Drug-Lab/Food Interactions: Drug- Serum K+ level with K+ supplements; effects of antihypertensive and lithium; Life threatening: Hyperkalemia if given with ACE inhibitor. Lab- Increase serum K+ level; may BUN, AST, alkaline phosphatase levels; serum sodium chloride.

Side Effects: N/V, diarrhea, rash, dizziness, H/A, weakness, dry mouth, photosensitivity. Adverse reactions: - Life threatening severity hyperkalemia, thrombocytopenia, megaloblastic anemia. Monitor signs and symptoms of K+ peaked T wave, Bradycardia, oliguria. Teach patient to avoid exposure to direct sunlight.

Ch 28 Coagulation modifier drugs

Thrombosis - Formation of a clot in an arterial or venous vessel. Arterial clots could be caused by stasis of blood, platelet aggregation (clumping) on vessel wall. They are usually made up of white & red clots. White clots: - (Platelets) initiating the process followed by fibrin formation trapping red blood cells into fibrin. Blood clots of the veins are from platelet aggregation with fibrin that attaches to red blood cells. Both kinds of thrombosis formation can become dislodged from the wall of the vessel and lead to embolus. Platelets dont usually stick together unless there is a break in the endothelial lining of the blood vessel. When platelets do stick to the lining they synthesize Thromboxane A2 (product of prostaglandins and protein synthesis). Platelet receptor protein glycoprotein IIb & IIIa. Thromboxane A2, and adenosine diphosphate (ADP) the activation of this receptor. As thrombus inhibits blood flow, fibrin, platelets and red blood cells surround the clot building the clots size and structure. As clots occludes the vessel, tissue ischemia occurs. The venous thrombus usually develops because of slow blood flow. Venous clots can occur rapidly. Heparin & Warfrin: Act primarily to prevent venous thrombosis whereas Anti-platelet drugs act to prevent ARTERIAL thrombosis. Both groups of drugs suppress thrombosis in general. Anticoagulants: Used to inhibit clot formation. They DO NOT dissolve clots like Thrombolytics. They are used in clients with venous & arterial vessel disorders that put them at high risk for clot formation. They can be administered Orally, Intravenously, or Subcutaneous. Venous- deep vein thrombosis, Pulmonary Emboli Arterial Coronary artery thrombosis (MI) presence of artificial valves, CVA/Strokes Heparin: Introduced in 1938, it is a natural substance found in the liver. It was used with blood transfusions to prevent clotting. Is indicated for a rapid anti-coagulant effect when thrombus occurs d/t DVT, Pulmonary Emboli, or an evolving stroke and for open heart surgery to prevent blood from clotting & in Disseminated Intravascular Coagulopathy. Heparin works with anti-thrombin III to inactivate Xa thus preventing thrombus formation. Poorly absorbed through the GI tract and much is destroyed by Heparinase (a Liver enzyme). IV bolus and or IV fluid for continuous drip Heparin prolongs clotting time. Heparin affects Partial Thromboplastin Time - (PTT). Heparin can platelet count causing Thrombocytopenia. ANTIDOTE: PROTAMINE SULFATE. Low Molecular Weight Heparin( LMWH) - Lowers the risk for DVT, Pulmonary Emboli after abdominal or orthopedic surgeries. Commonly used to prevent Pulmonary Emboli. LMWHs produce more stable responses at recommended doses, therefore frequent monitoring of PTT is not required. LMWH inactivates factor Xa , but it is less able to

inactivate thrombin like Heparin is able to. 1. 4 Types of LMWH are: All can be given subcutaneously and do not require monitoring of aPTT. Treatment is injection in the abdomen for 7-14 days. It is usually started in the hospital 24 hrs. post-operatively. The half life of LMWH are 2 to 4 times longer than that of heparin. Instruct clients not to take aspirin or other anti-platelet drugs while on LMWH. Bleeding with these drugs is less likely to occur than with Heparin. If bleeding dose occur Protamine Sulfate is the anti-dote.(dose would be 1mg of Protamine S. for every 1mg of LMWH given.) Contra-Indications: Pt. whom have had a stroke, peptic ulcers, or other blood anomolies Enoxaparin Sodium: (Lovenox) Dalteparin Sodium: (Fragmin) Danaparoid : ( Orgaran) - **It is considered LMWH but actually does not have Heparin in its structure. d. Tinzaparin Sodium: (Innohelp)

low molecular weight heparin....Lovenox used to prevent DVT for post-op, prevents acute event, lowers risk of bleeding.HIGH ALERT DRUG!!! SE: fever, confusion,nausea, thrombocytopenia,bleeding.DONT MIX WITH OTHER DRUGS=increase risk of blleding...ASSESS for bleeding. SUBCUT ONLY.Teach soft toothbrush.leave bubble in syringe.LOVE handles

Direct Thrombin Inhibitors: Anticoagulants II There are 4 new parental anti-coagulants that directly inhibit thrombin from converting fibrinogen to fibrin. Three are given Intravenously and are very costly! Argotroban ( Acova) Bivalirudin (Angiomax) binds with inhibitors free flowing thrombin Lepirudin (Refludan) The 4th Drug is given Subcutaneously Desirudin (Iprivask) C. Oral AntiCoagulants- Examples would be Warfrin/Coumadin before it was used on humans it was used on rodenticides to kill rats by causing them to hemorrhage. Oral anti-coagulants inhibit hepatic synthesis of Vitamin K thus affecting clotting factors II, VIII, IX, and X. Warfrin is used mainly to prevent thromboembolic conditions such as: 1. Thrombophlebitis 2. Pulmonary Embolism 3. Embolisms formation caused by Aterial Fibrillation which can lead to CVA Prolong clotting time and monitoring of Prothrombin Time . INR = International Normalized Ratio is used to account for the varibilities in reported levels from different labatories. Normal INR is 1.3 to 2 however patients on Warfrin therapeutic range is 2-3 INR and for patients with Mechanical Heart Valves INR is maintained at 2.5-3.5 and could go as high as 4 on the INR.

Coumadin PO inhibits hepatic synthesis of VIT k dependent factors .Use for chronic A-Fib, prosthetic heart valves, CHRONIC anticoagulation needs:prevents or slows the action of blood

clots. LABS:PT & INR(2-3) ANTIDOTE: Vit K. SE: anorexia, bleeding, heamaturia, thrombocytopenia, hemmorrhage. assess for bleeding-stools & GI. AVOID foods rich in VIT K(leefy greens)no ASA and NSAIDS
Coumadin has a long t and a very long duration. Drug accumulation can occur and lead to external and internal bleeding. Teach patients to watch for signs of bleeding(petechiae, ecchymosis, tarry stools, & hematemsis. ANTIDOTE FOR COUMADIN IS VITAMIN K or Aquamephyton-but it takes 24-48 hrs to be effective. Usually a low dose of oral Vitamin K is recommended for patient with INR of 5.5. ** If excessive Vitamin K is given it may take Warfrin 1- 2 weeks before it can be effective again. If patient with acute bleeding give Fresh Frozen Plasma. D. Anti- Platelet Drugs: are used to prevent thrombosis in the arteries by suppressing platelet aggregation. (Heparin and Warfrin are used to prevent thrombosis in the veins). Anti- platelet drug therapy is mainly for prophylactic use in : 1. Prevention of myocardial infarction or stroke for patients who have a family history. 2. Prevention of a repeat M.I. 3. Prevention of a stroke in patients who have had a transient ischemic attack. Long term therapy of a low dose aspirin has been found to be both an effective and cheap treatment for suppressing platelet aggregation. Aspirin works by inhibiting cyclooxyganase, an enzyme needed by the platelets to synthesize thromboxane (A2). Because aspirin has a prolonged anti-platelet activity it should be stopped/discontinued for at least 7 days prior to surgery. 1. Other Examples of anti-platelets: a. Dypridamole (Persantine) b. Ticlopidine (Ticlid) c. Clopidogrel (Plavix) Prototype It may be prescribed by itself or in combination with Aspirin. Tirofiban (Aggrastat) Clopidogrel, dypridamole and ticlopidine have similar effects as aspirin but they are known as Adenosine Diphosphate antagonists affecting platelet aggregation. 2. Clopidogrel (Plavix) Anti- Platelet Used to prevent recurrence of MI, CVA, vascular death. Pregnancy Category: B Usual PO dose is a loading dose of 3oomg then 75 mg. A. Pharmacokinetics: 1. Absorption: Rapid 2. Distribution: (Protein Bond) 94%-98% 3. Metabolism: t : 8 hours 4. Excretion : 50% in urine and 50% in feces B. Pharmacodynamics: PO: Onset- 12 hrs. Peak- 2 -3 Duration: 3 days or longer. Side Effects- Upper Resp. Tract Infection, flu-like symptoms, dizziness, headaches, fatigue, chest pain, diarrhea Adverse Reactions: None of significance May cause hypertension, bronchitis. Thrombolytic: Remember that normally it takes about 1-2 weeks for a blood clot to disintegrate by natural fibrinolytic mechanisms. Our goal with thrombolytic therapy is for this to occur much quicker thus preventing ischemia & then tissue necrosis. These drugs work by promoting the mechanism of converting plasminogen to plasmin, which destroys the fibrin in blood clot. The thrombosis will disintegrate within 4 hours after the administration of a thrombolytic drug. These drugs should be administered within 3 hours of a thrombolytic

stroke. They are also used in treatment of Pulmonary Emboli, & Deep Vein thrombosis. 1. Five Types of Thrombolytics: 1. Steptokinase- enzyme 2.Urokinase- enzyme c. Alteplase- alos know as a tissue plasminogen activator(tPA) Prototype) d. Reteplase (Retavase) e. Tenecteplase(TNKase) *** all five of these drugs induce Fibrinolysis (fibrin breakdown) ** Anticoagulants and Anti-platelets increase the risk of hemorrhage Alteplase: promotes the conversion of plasminogen to plasmin. Thrombolytic agent. It Initiates fibrinolysis Trade name: tPA, Activase Adult Dose: IV Bolus 15mg, then 50mg infused over 30 minutes, then 35mg infused over 60min. Maximum; 100 mg Drug- Lab Food Interactions: Drug: Increase bleeding when taken with oral anticoagulants, NSAIDS, cefotetan, plicamycin Lab; Decreases in plasminogen, fibrinogen, hematocrit, and hemogloblin 1. Pharmacokinetics: a. Absorption: IV b. Distribution: Protein Bind Unknown c. Metabolism: t1/2- 5min d. Excretion: Urine 2. Pharmacodynamics: PO Onset: immediate Peak: 5-10 min. Duration: 3hrs 3. Side Effects: Bleeding 4. Adverse Reactions: Life-threatening: Intracerebral hemorrhage, stroke, atrial or ventricular dysrhythmias. 5. The Antithrombolytic drug Aminocaproic Acid(Amicar) is used to stop bleeding by inhibiting plasminogen activation, which inhibits thrombolysis.

Ch 29Anti-Lipidemics And Peripheral Vasodilators

There are 4 major categories of lipoproteins: 1High Density Lipoproteins= HDL AKA Friendly or Good lipoproteins. It is responsible for removing cholesterol from the blood stream and sending it to the liver for excretion in the bile. 2. Low Density Lipoproteins= LDL= Bad Cholesterol contains 50- 60% of the cholesterol in the blood stream. With an elevated LDL there is a greater risk for developing atherosclerotic plaques and heart disease. 3. Very Low- Density Lipoprotein= VLDL- they carry mostly triglycerides & less cholesterol. 4. The first treatment for hyperlipodemia should be a reducing the intake of saturated fats and cholesterol in the patients diet. The plan is to reduce total intake of fats to 3040% of intake and reduce cholesterol intake to 300mg/day. **Remember that 75-80% of our total cholesterol is produced Endogenously. ** Diet modification will only reduce cholesterol levels by 10%- 30%. Exercise is another important non-pharmacuetical way to work on for lowering cholesterol levels. Exercise will increase the HDL and lower cholesterol levels.

Smoking increase the LDL, cholesterol and decreases the HDL. Antilipidemics: Drugs that lower lipoproteins. Lipids (Cholesterol, triglycerides, and phospholipids) are bound in the inner shell of protein, which is a carrier that transports lipids into the blood stream. Hyperlipidemia is defined as an excess amount of one or more lipids in the blood stream. Drugs that lower lipid levels include bile-acid sequestrants, fibrates (fibric acid), nicotinic acid, cholesterol absorption inhibitors and hepatic 3 hydroxy-3methylglutarycoenzyme A reductase inhibitors (statins). The statins have fewer adverse effects and are tolerated well. Clients need to be educated that if they stop Antilipidemic therapy that their cholesterol levels will go back to pretreatment levels. Questran One of the first bile sequestrants, which reduces LDL. It binds with bile salts in the intestines. It can be used with Statin drugs .It is a gritty powder that must be dilated in liquid like water or juice. Clofibtate (Atromid- S) & Gemfibrizol( Lopid)- are fibratic acid derivatives that are more effective in lowering triglcerides and VLDL. They are highly protein bond and should not be taken with anticoagulants. It is not suggested for long term use d/t many side effects like cardiac dysrhythmias, angina, thromboembolism, and gall stones. Nictotinic Acid-(Niacin)or (Vitamin B2)- reduces VLDL& LDL. Because of its numerous side effects and need for larger doses ( al low as 20% of clients can tolerate it. Ezetimibe (Zetia)- is a cholesterol absorption inhibitor that acts on the cells in the small intestine to inhibit cholesterol absorption. It lowers levels of cholesterol and lipids from the foods that are ingested. It lowers LDL, triglycerides, and ApoB levels. It also causes small increase to the HDL. It MUST be combined with statins for optimum effect. Statins- first introduced in 1987, inhibits the enzyme HMG CoA reuctase in cholesterol synthesis in the liver. These drugs decrease the concentration of cholesterol, decreases the LDL, and slightly increased HDL. May see a decrease in LDL in as early as 2 weeks. All statins should be monitoring Liver enzymes and yearly eye examinations because of risk of cataract formation and rhabdomyolysis. 1. Atorvastitin Calcium (Lipitor) Prototype 2. Fluvastain (Lescol) 3. Lovastatin (Mevacor)- 1st statin to be used . Side effects: GI disturbances, H/A, muscle cramps, and tiredness . 4. Pravastatin Sodium ( Pravachol) 5. Simvastatin (Zocor) 6. RosuvastatinCalcium (Crestor) Atrovastatin( Lipitor)- Decreases LDL by 25% with lower doses and 55% with higher doses. It inhibits HMG-CoAreductase, the enzyme necessary for hepatic production of cholesterol. Adult PO : 10mg/day may increase up to 80mg/day. Drug Lab-Food Interactions: Drug: Decrease effect with antiacids, propanolol. May increase digoxin level, oral contraceptives. Increases effects with macrolide antiobiotics, and antifungals. 1. Pharmacokinetics; a. Absorption: rapid b.

Distribution: Protein bond 98% c. Metabolism: t1/2 14 hours: metabolites 20-30 hrs. d. Excretion: to primarily in bile; some in urine Pharmacodynamics: PO onset: 2 week for decreasing cholesterol Peak: 1-2 h. 2-4 weeks to be effective Duration: 24 hrs. 3. Side effects: Rare H/A, rash/pruitus, constipation/diarrhea, sinusitis, pharyngitis 4. Adverse Reactions: Rhabdomyolysis, myalgia, photosensitivity, cataracts It can be used and tolerated by some whom concomitant use of Aspirin.

Ch 25Antihypertensive drugs Ch 26Diuretic drugs Hypertension is defined as an increase in systolic B/P > 140 and the diastolic > 90 mmHg.
Essential HTN: affecting 90 % of persons with HTN exact origin of essential HTN is unknown. A. Contributing Factors- Family Hx of HTN Hyperlipidemia African American background- Diabetes Obesity Aging Stress Excessive smoking and alcohol Secondary HTN- it is the other 10% of HTN cases are related to Renal & Endocrine disorders Kindeys regulate the Reni- Angiotension I to Angiotension II-(causes release of Aldosterone from the Adrenal glands). Baro-receptors in the Aorta and Carotid Sinus and the vasomotor in center of the medulla assist in regulating B/P. Catecholamines Norepinepherine released from sympathetic nerve terminals and Epinepherine released from the Adrenal Medulla B/P through vasoconstriction activity on the blood vessels. Anti- Diuretic Hormone (produced by hypothalamus by stored and ANP (atrial naturetic peptide and Brain Naturetic Peptide) released by the posterior pituitary gland. Non- Pharmacologic Control for HTN : If systolic is > 140 anti hypertension drugs are generally necessary. A. Stress reduction techniques B. Exercise C. Salt restriction D. Alcohol ingestion E. Weight reduction Most Clients may need two or more Anti - hypertensive drugs to achieve a goal Blood pressure reading: 1. Six Categories of drugs to treat HTN: 1. Diuretics- ** see chapter 41 2. Sympatholytics-(Beta Adrenergic Blockers) 3. Direct- acting Arteriolar Vasodilators4. Angiotension Convert Enzyme inhibitors5. Angiotension II receptor Blockers 6. Calcium Channel Blockers Beta Adrenergic Blocker : Beta ( 1 & 2) Adrenergic Blockers reduce cardiac output by

diminishing the sympathetic nervous system response to basal sympathetic tone. They reduce heart rate, contractility, and Renin release. African Americans with HTN do NOT respond as well to Beta blockers for HTN control so they are given beta blockers combined with diuretics. 1. Metroprolol (Lopressor, Toprol SR)- Beta1 {Prototype}PO Adult dose for HTN 50-100mg/d in 1-2 divided doses Maintenance dose is 450mg/day in divided doses. Elderly- PO 25mg/day Maintenance dose of 25300mg/day Myocardial Infarction- PO: 100mg B.I.D. IV: 5mg q 2 min X 3 doses. Drug- Lab/Food Interactions: Drug- bradycardia with digitalis: Hypotensive effect with other anti-hypertensive, alcohol, anesthetics. a. Pharmacokinetics : 1. Absorption: PO 95% 2. Distribution: Protein Bound is 12% 3. Metabolism: t1/2= 3-7 hrs. 4. Excretion : in urine b. Pharmacodynamics: PO : Onset 15 min IV Onset: Immediate Peak: 1.5 hrs IV Peak : 20 min Duration: 10-19 hrs. IV Duration: 5-10 hrs. c. Side Effects: Fatigue, weakness, dizziness, nausea, vomiting, diarrhea, mental changes, nasal stuffiness, impotence, libido, depression. d. Adverse Reaction: Bradycardia, thrombocytopenia e. Life Threatening: Complete heart block, bronchospasm, and agranulocytosis. Cardioselective Beta-blockers- are preferred Beta Blockers because they act mainly on the cardiac Beta1 receptors rather than Beta2 so bronchoconstriction is less likely to occur. Medications in this group are: Acebutolol ( Sectral), Atenolol ( Tenormin), Betaxolol( Kerlone), Bisoprolol (Zebeta). 2. Centrally Acting Alpha2- Centrally acting alpha2 agonists the sympathetic response from the brainstem to the peripheral vessels. By stimulating the alpha2 receptors which in turn sympathetic activity: vagus activity, cardiac output and serum epinephrine, norepinepherine, & renin release. All actions result in reducing peripheral vascular resistance and vasodilation. This group of drugs has minimal effect on cardiac output and kidney perfusion. Beta Blockers are NOT given with centrally acting sympatholytics, because of bradycardia during therapy and rebound hypertension on discontinuing therapy that can occur. Example: Of these types of drugs is Methyldopa (Aldomet). In higher doses Methyldopa & clonidine can cause water retention therefore they should be used with a diuretic. Potential side effects: drowsiness, dry mouth, dizziness, and slow heart rate(bradycardia). Methyldopa should NOT be used in clients with impaired liver functions & serum liver enzymes should be monitored periodically. These drugs must not be stopped abruptly d/t rebound hypertensive crisis. 3. Alpha-Adrenergic Blockers: - These drugs block the alpha receptor sites resulting in vasodilation B/P. Useful in treat of HTN in patients with Hyperlipidemia. They the very low density lipoproteins (VLDL) and the low density lipoproteins (LDL) which cause plaque buildup leads to artherosclerosis, they also build up the good lipoproteins High

density ones (HDL). They are also good for diabetic patients because they do not effect Glucose metabolism. 4. Examples of Alpha Adrenergic Blockers: Prazosin (Minipres) {Prototype}, Terazosin( Hytrin), Doxazosin( Cardura) are mainly used for HTN but can also be used for treatment of Ben usually are given once/day. They do cause NA+ & water retention therefore a diuretic is also given concomitantly to fluid accumulation. More potent medications like Phenoxybenzamine and Tolazoline are used to treat HTN Crisis & vere HTN resulting from catecholamine secreting tumors of the adrenal medulla like (phenochromocytomas). Prazosin HCL (Minipres) Alpha Adrenergic Blocker PO Adult dose 1mg B.I.D. or T.I.D. With a maintenance dose of 3-15mg/day. Drug- lab/ Food Interactions: Hypotension effect with other anti-hypertensives, nitrates and alcohol. a. Pharmacokinetics : Absorption in G.I. 60%, 5% in circulation 1. Distribution: Protein Bond 95% 2. Metabolism: 3 Hours 3. Excretion: in bile & Feces 10% in urine. 4. Mode of Action: Dilation of peripheral blood vessels via blocking Alpha Adrenergic receptors. 2. Pharmacodynamics: P.O. Onset o.5 2 hrs. Peak: 2-4 hrs. Duration: 10 hrs. a. Adverse Reactions: Orthostatic Hypotension, palpitations, Tachycardia, pancreatitis b. Side Effects: Drowsiness, H/A, N/V, diarrhea, impotence, vertigo, urinary frequency, tinnitus. c. Drug Interactions: when Alpha Adrenergics Blockers are taken with Antiinflammatory drugs and nitrates Fluid Retention peripheral edema Nitrates - Lower B/P as do Alpha-Adrenergic which leads to syncope/fainting. Adrenergic Neuron Blockers are potent antihypertensive drugs that block Norepinepherine. Release from the Sympathetic nerve endings, causing a decrease in B/P, & decrease in Cardiac output & in peripheral vascular resistance. Reserpine, Guanethidine, Guanadrel (are 3 very potent drugs) that are used to treat severe HTN. Adrenergic Neuron Blockers are the LAST drugs considered for treatment of HTN because of the orthostatic hypotension. Reserpine can cause nightmares and suicidal tendencies. Alpha1, Beta1, Adrenergic Blockers : Labetalol( Normodyne) & Carteolol(Cartrol) are examples of Alpha/Beta blockers. When the Alpha1 receptor sites are blocked it causes Vasodilation. , which decreases the resistance of the blood flow. The blocking of effect on the Alpha receptor site is stronger than that on the Beta receptor therefore B/P is lowered and pulse rate is moderately decreased. Common side Effects: Orthostatic Hypotension, GIdistrubances, nervousness, dry mouth, fatigue. *** Large doses of Labetalol may cause Atrial Ventricular Heart Block. (Property of Beta blockers that slows Atrial Ventricular conduction which in turn slows heart rate). Direct Acting Arteriolar Vasodilators: This group of drugs act by relaxing the smooth muscle of mainly the arterioles. Vasodilatation leads to blood flow to the Brain and kidneys, with a decrease in B/P Na and water are retained leading to edema. This is why a diuretic would be given with these drugs. Examples would be Hydralazine and Minoxidil both can be

used to treat mild to moderate HTN. Also because of the vasodilatation that these drugs cause Reflex Tachycardia and Renin is released. Beta Blockers are frequently prescribed with D.A.A. V. to decrease the Heart rate (counter act the Reflex Tachycardia). Nitroprusside & Diazoxide : These are 2 very potent vasodilators used for acute HTN emergency. Nitroprusside acts on both arterial & venous blood vessels, whereas Diazoxide acts on only arteries. Common side effects: Hydralazine side effects are tachycardia, palpitations, edema, nasal congestion, H/A, dizziness, bleeding, and Lupus like symptoms. Minoxidil & Diazoxide : Refex Tachycardia, palpitation, restlessness, agitation, nausea, and confusion. Diazoxide: hyperglycemia due to its action of inhibiting release of insulin from the Pancreatic Beta cells. Angiotension Converting Enzyme Inhibitors: They inhibit the formation of Angiotension II and blocks the release of Aldesterone. When aldesterone is blocked Na and water are not retained but are excerted. K + is retained. ACE inhibitors cause little change in Cardiac Output or HR but do peripheral vascular resistance. These drugs can be used in patients with renin levels. They are primarily used to treat HTN , some are effective in treatment of Heart Failure. There are 10 drugs in this category: 1. First one discovered in 1970s is Captopril (Capoten) 7. Moexipril(Univasc) 2. Benzepril (Lotension) 8. Perindopril (Aceon) 3. Enalapril (Vasotec) 9. Fosinopril (Monopril) 4. Ramipril(Altace) 10. Quinapril (Accupril) 5. Trandolapril(Mavik) 6. Lisinopril (Prinavil Zestril) These drugs can be used as the first line Anti Hypertensive agents but the use of Thiazide diuretics are also recommended. ****** African Americans and Older Adults DO NOT RESPOND TO ACE inhibitors until diuretics are added. SHOULD NOT PRESCRIPED/ADMINISTERED DURING PREGNANCY (D/T the effect they have of reducing Placental blood flow). Side Effects: Constant irritating cough; Nausea/Vomiting, diarrhea, H/A, dizziness, fatigue, insomnia, Hyperkalemia, and tachycardia. Contraindications: Should not be administered while pregnant will cause fetal harm d/t decrease placental blood flow. Should not be taken with K+ sparing diuretics or salt substitutes (those that use K instead of Na). Angiotension II Receptor Blockers (ARBs): They are similar to the ACE drugs except ARBs block Angiotension II from Angiotension receptors found in many tissues. ARBs cause vasodilatation and peripheral resistance. They do not cause the constant irritating cough. ARBs should not be taken during pregnancy either. Examples: Losartan (Cozaar), Valsartan (Diovan) Irbesartan (Atacand), Olmesaran Medoxomil (Benecar)- these agents block the vasoconstrictor effects of Angiotension II at the receptor sites. ARBs can be used as a first line Treatment for HTN. Pharmacokinestics: Cozaar is used primarily to manage HTN and to form active metabolites. 1. Distribution: They are Highly Protein Bond 2. Metabolism: t 1.2- 2 hours & metabolite half life is 6- 9 hrs. 3. Excretion: In the Urine and Feces

Pharmacodynamics: Losartan (Cozaar) is a potent vasodilator which blocks the binding of Angiotension II to the Angiotension receptors found in many tissues. PATIENTS WITH MILD HEPATIC INSUFFICENCY CAN TAKE THESE DRUGS. The Peak time is 6 hrs., Duration is 24 hrs. THEY ARE LESS EFFECTIVE IN AFRICAN AMERICAN and may cause Angioedema Direct Renin Inhibitors: Aliskiren ( Tekturna) 1st FDA approved Renin inhibitor. Aliskiren binds with Renin causing a in Angiotension, Angiotension II and Aldesterone levels. Effective for the treatment of mild to moderate HTN. Can be used alone or with another antihypertensive agent. Has an added effect in B/P when combined with Thiazide diuretics or ARBs. Losartan ( Cozaar) Angiotension II receptor Blockers . Pregnancy C ( First Trimester), D (2nd or 3rd Trimester can use Hyzaar). PO: For HTN- 25- 50 mg/day in single or divided doses. Maxium dose is 100mg/ day. Contraindicated: During Pregnancy and while Breastfeeding Caution: Renal & Hepatic Impairment. Pharmacokinestic: 1. Absorption: Rapidly absorbed in blood in 25-30 minutes. 2. Distribution: Protein bond 90-95% 3. Metabolism: t 1.2- 2 hrs. metabolites in 6-9hrs. 4. Excretion: 35% in the urine. 5. Side Effects: Dizziness, diarrhea, insomnia, & occ. Cough 6. Drug & Lab Interactions: Phenobarbital effect of Cozaar & its metabolites May increase ALT, AST, ALP ,Bilirubin , Creatinine , Hbg. and Hct. 7. Adverse: Upper Respiratory Infections. Pharmacodynamic: Onset: < 1 hr. Peak : 6 hrs. Duration: 24 hrs. Calicum Channel Blockers: These are a group of drugs that are slow channels found only in myocardium & vascular smooth muscle. Free Ca+ muscle contractility, peripheral resistance, & B/P. Ca+ channel blockers also called Calcium anti-agonist promote vasodilation. Large central arteries are not as sensitive to Ca+ as the coronary, Cerebral and peripheral arteries are. They are highly protein bond but have a short half- life. 3 groups of Ca+ blockers. Calcium Channel Blockers lower B/P better in African Americans than drugs in other categories. 1. Verapamil (Calan): is used for treatment of chronic HTN, angina pectoris & cardiac dysrhythmias. Verapamil and Diltiazem act on the arterioles & the heart. Nifedopine is used to prevent ischemic brain injury due to vasospasm that often accompanies subarachnoid hemorrhage. Also used as treatment of choice in Variant angina (Prentz Metal ) also thought to be caused by vasospasm of the coronary arteries. 2. Nifedipine (Procardia): Decreases B/P in older adults & in those with low serum Renin values. In the immediate released capsules (10-20mg) it has been associated with increased incident of sudden Cardiac Death especially when prescribed for outpatient at high doses d/t the fact that Ca+ channel blockers cause reflex tachycardia. This tachycardia is more prevalent with Procardia. 3. Amlodipine (Norvasc) : It is used to treat mild to mod. HTN, and Angina Pectoris. Mode of action: Decreases peripheral vascular resistance (vasodilation),

promoting in B/P. PO 5- 10mg/day or for Elderly 2.5- 5mg/day. Lotrel is a combination of Amlodipine with Benzepril. Contra-Indications: Severe hypotension. Cautious Use: Liver Disease, Heart Failure, Aortic Stenosis, pregnancy & lactation. Drug- Lab Interactions: Drugs bradycardia with Adenosine Labs: May Amlodipine with Grapefruit juice. 1. Pharmacokinetics: a. Absorption: > 90% is absorbed; gradually absorbed from the G.I. tract. b. Distribution: Highly Protein Bond > 95% c. Metabolism: t 30- 50 hrs. Elderly: t : 50100 hrs. d. Excretion: in urine & feces as inactive metabolites. 2. Pharmacodynamics: Onset is gradual Peak: 6-9 hrs. Duration 24 hrs. Usually only prescribed once a day. 4. Side Effects : Peripheral edema may occur because of its vasodilator effect, flushing, dizziness and nausea. 5. Adverse: Reflex Tachycardia

Ch 27 Fluid and electrolytes Ch 30 Pituitary drugs Ch 31 Thyroid and antithyroid rugs Ch 32 Antidiabetic drugs Ch 33 Adrenal drugs Ch 34 Womens health drugs Ch 11 Analgesic drugs Ch 12 General and local anesthetics Ch13 CNS depressants and muscle relaxants

Sedatives/Hypnotics: Often are prescribed for treatment of insomnia Remember that dreams occur during Rapid Eye Movement stage of sleep. A. They are the mildest form of CNS depressants are our sedative drugs. B. They do not affect the consciousness. Barbiturates 1900s were introduced as a sedative. A. Long acting - Phenobarbital B. Intermediate Acting- Butabarbital (Butisol) C. Short- Acting Secobarbital ( Seconal) & Pentobarbital (Nembutal) {Prototype} D. Ultra Short Acting- Barbiturate, Thiopental (Na Pentothal) Benzodiazepines minor tranquilizer or anxiolytic. Class IV according to Controlled Substances Act. They the action of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) to the GABA receptors. Neuron excitability is . Also of the Benzodiazepines except temezepam can cause vivid dreams/nightmares. Should not be used for longer than 3 to 4 weeks. Remember that it is recommended that with renal or hepatic dysfunction smaller

doses A. Chlordiazepoxide (Librium) class IV. Used also for treatment of alcohol withdrawl syndrome DTs, anxiety and tension. For anxiety usual PO dose is 5-25mg t.i.d. or q.i.d. For alcohol withdrawl PO/IM/IV 50-100mg max. 300mg/d B. Flurazepam (Dalmane) {Prototype} C. Temazepam (Restoril) D. Triazolam ( Halicon) E. Lorazepam (Ativan) {Prototype} used for treatment of mild to moderate anxiety. PB 85-95%, t 3.5- 21 hr. F. Diazepam (Valium) used to manage anxiety, muscle spasms status post epilepticus. PO/IM/IV 2-10mg b.i.d.- q.i.d. For Post epilepticus IV 5-10mg q 10-20 min. 30mg

max.

Non benzodiazepines Used for short term insomonia (< 10 days duration) a. Zolpidem (Ambien) .Duration is 6-8 hrs. with a short t1/2 of 2 to 2.5 hrs. M a. Metabolized in the liver to 3 inactive metabolites and excreted in bile, urine, and feces. Chloral Hydrate- It is used to induce sleep and decrease nocturnal awakenings. Fewer occurrences of hang-over, resp. depression, and tolerance. Effective in older clients. It can be given to patients with mild hepatic dysfunction, but should be avoided if liver or renal failure is severe. Anesthetics - Two classifications 1. General Anesthetic depresses the CNS, alleviates pain, and causes loss of consciousness. One of the first ones used was Nitrous Oxide (laughing gas) 1. Four Stages of Anesthesia1st stage is Analgesia (induction stage) (consciousness and goes to loss of consciousness. Loss of sensation of smell and pain occur. 2. 2nd stage is Excitement Or Delirium produces loss of consciousness caused by depression of the cerebral cortex. Confusion, excitement or delirium occurs. 3. 3rd stage Surgical Surgical procedure is performed during this stage. 4. 4th stage Medullary Paralysis Toxic stage of anesthesia Resp. are lost & circulatory collapse occurs. Must be on Ventilator. 2. Inhalation Anesthetics- used during the 3rd stage, inhalation gases are used. Some like Nitrous Oxide are absorbed quickly, have rapid action but also eliminated quickly. Some examples in the 1950s and later are Halothane, Methoxyflurane, Enflurane ,Isoflurane, Desflurane, and in 1995 Seroflurane. Inhalation agents are usually combined with a barbiturate, a strong analgesic like morphine, and a muscle relaxant like pancuronium. Potential adverse effects are respiratory depression, hypotension, dysrhythmias,& hepatic dysfunction.ould be used. 3. Intravenous Anesthetics May be used for induction with addition of inhalation anesthesia or in an outpatient setting for procedures with an anticipated short surgical time. a. Midazolam (Versed) b. Propofol (Diprivan)- this drug supports microbial growth & may risk for infections. Open vials should be discarded after 6 hours to prevent sepsis.

4. Topical Anesthetics- Available in many different forms. Decrease the sensitivity of the nerve endings to the affected/injured area. 5. Local Anesthetics These drugs block pain at the site where the drug is administered, allowing for consciousness to be maintained. Beneficial in many minor procedures. Consist of two main groups Esters and Amides. a. Esters Short Acting - Chloroprocaine (Nesacaine), Procaine HCl (Novacain) which both is effective for (1/2-1hr.). Long Acting -Tetracaine (Pontocaine), which is effective for (3-10 hr.) b. Amides Low incident of allergic reactions. Lidocaine Hydrochloride (Xylocaine) has a rapid onset and long duration of action. Labeled as Moderate acting (1-3 hr.) Another example would be Prilocaine (Citanest). Long Acting Bupivacaine (Marcaine & Sensorcaine) 6. Spinal Anesthesia use of local anesthetics injected in the subarachnoid space at L3-4. Potential complications could be respiratory distress if anesthetic is injected or travels to high in the spinal column, headaches due to leak of cerebral spinal fluid. a. Spinal Nerve Block local anesthetics is injected into the 2nd layer of the spinal column subarachnoid membrane b. Epidural Block- local anesthetic is injected into the outer covering of the spinal column the dura mater. c. Caudal Block- anesthetic is placed near the sacral area. A d. Saddle Block anesthetic placed near the lower end of the spinal column to numb the perineal area.
Ch 30 - 32

The endocrine System consists of ductless glands that secrete hormones in the blood stream. Endocrine glands include: Pituitary (Hypophysis), Thyroid, Parathyroid, Adrenal , gonads, and the Pancreas. Hormones are chemicals synthesized from amino acids & cholesterol that act on body tissue, organs & affect cellular activity. Glands- A. Pituitary Gland- Located at the base of the brain. Divided into 2 lobes Anterior and Posterior. 1. Anterior Lobe: (Adenohypophysis) Often called the Master Gland D/T its function of secretions of hormones that stimulate the release of other hormones from target glands like the thyroid. Parathyroid, adrenals, and gonads. It secretes a total of 6 hormones a. Thyroid Stimulating Hormone (TSH) also called Thyrotropic Hormone - is secreted in response to the Hypothalmus releasing Thyroid Releasing Hormone. When this hormone is over secreted (hypersecretion) can cause Hyperthyroidism. b. Adrenocorticotropic Hormone ( ACTH)- Hormone secreted to stimulate Adrenal Cortex to release Glucocorticoid (cortisol), Mineralcorticoid hormone( Aldesterone). More ACTH is secreted in the AM then in the PM c. Gondtropins- Follicle stimulating hormone (FSH), & Luteinizing Hormone (LH) these hormones control the release of hormones from the Thyroid and Adrenal, and ovaries. Regulate hormone secretion from the ovaries & testes. d. Growth Hormone (GH)or the Somatotrophic Hormone acts on body tissues, particularly the bones & skeletal muscles. Regulated by the amount of Growth Hormone Releasing Hormone & Growth Hormone

Inhibiting Hormone (Somatostatin) that is released from the Hypothalamus. Sympathomimetics drugs, Serotinin, glucocorticoids can inhibit the secretion of Growth Hormone. e. Prolactin (PL)- stimulates milk formation in the glandular breast tissue after childbirth f. Melanocyte Stimulating Hormone (MSH) Remember the amount of each hormone is regulated by negative feedback system to the Anterior Pituitary Gland. Posterior Lobe: (Neurohypophysis) secretes 2 Neurohormones: A. Antidiuretic Hormone- Increases the reabsorbtion of water in the tubules, returning it to the systemic circulation. Secretion of ADH is regulated by serum Osmolality .If serum osmolality is increased so is the production of ADH. (Vasopressin). B. Oxytocin- Stimulates the contraction of the smooth muscles of the Uterus. Thyroid Gland- It also has 2 lobes and is located on either side of the anterior Trachea. It secretes two hormones: A. Thyroxine (T4) B. Triiodothyronine( T3) These hormones affect nearly every tissue & organ by controlling their metabolic rate. Stimulation by the Thyroid hormone results in cardiac output, O2 consumption, carbohydrate use, protein synthesis, & the breakdown of fats (Lipolysis). These hormones also affect body heat regulation and womens menstrual cycles.\ . Parathyroid Gland: There are 4 parathyroid glands 2 pairs that lie on the dorsal surface of the thyroid gland. It secretes 2 hormones A. Parathyroid Hormone/PTH - this hormone regulates serum Ca+ levels. When there is a in serum Ca+ (Hypocalcemia)the PTH is release from the parathyroid gland. PTH will serum Ca+ levels by: 1) Mobilizing Ca+ from the bone. Remember PTH P for PTH pulls Ca+ from the bone and puts it back into the blood stream; 2).Promotes Ca+ absorption from the intestines; 3) Promotes Ca+ re-absorption from the renal tubules. B. Calicitonin- Hormone that primarily is produced by Thyroid (and to a lesser extent the Parathyroid & Thymus Glands). Its purpose is to inhibits Ca+ re-absorption by the bone & renal excretion of Ca+ . Think Calcitonin Keeps Calcium in the bone, which is the opposite effect of P.T.H. Adrenal Glands: Located at the top of each Kidney. There are two separate sections: A. Medulla or Center secretes catechlomanines Epinephrine and Norepinephrine. B. Cortexor known as the outer portion of the gland. Secretes 2 major hormones: 1. Glucocorticoids- Principal hormone is Cortisol 2. Mineralcorticoid- Aldersterone which acts in the kidney telling the kidney to reabsorb Na+ and then water back in the systemic circulation. Some other hormones to a smaller extent would be Androgen, Estrogen, and Progestin. Pancreas: Located to the left and behind the stomach is both an Exocrine and Endocrine gland. A. Exocrine property would be the secretion of digestive enzymes into the duodenum of the small intestines. B. Endocrine- hormones are secreted by cluster of cells called Islets of Langerhans There are 2 types of cells the Alpha islet cells produce

glucagon(which breaks glycogen down into glucose in the liver). The Beta islet cells secrete Insulin (Regulates glucose metabolism). Growth Hormones: There are 2 which are secreted from the Hypothalamic Hormones: A. Growth Hormone- releasing Hormone and Growth Hormone Inhibiting Hormone (Somatostatin). Growth Hormone doesnt have a specific target gland but it does affect body tissues and bones. Synthetic Growth Hormone Drugs cannot be given orally due to them being inactivated by gastric enzymes. They are given subcutaneously or intramuscularly. G.H. replacement therapy is very expensive. G.H. acts on newly forming bone and it must be administered before the epiphyses are fused. Prolonged G. H. therapy can antagonize Insulin secretion and eventually cause Diabetes Mellitus. A. G. H. Deficiencies Drug Therapy: Drugs used to treat growth failure in children are : 1. Somatrem (Protropin)- Has identical amino acid plus an additional amino acid. 2. Somatropin (Humatrope) has identical amino acid sequences as Human G Hormone (contraindicated in children with Prader Willi Syndrome and those children who are severely obese or who have Respiratory impairment. B. Growth Hormone Excess- Gigantism- excessive growth during childhood or Acromegaly (excessive growth after puberty) can occur with Hypersecretion of G.H. and is associated with Pituitary tumors. If the treatment with radiation is ineffective the Prolactin- Release Inhibitor: Bromocriptine can inhibit the release of G. H. C. Octreotide(Sandostatin) : is a potent synthetic Somatostatin used to suppress G.H. release. It can be used alone or with Surgery and or Radiation. This drug is expensive. G.I. side effects are common. This drug can also be used for severe diarrhea resulting from carcinoid tumors. Thyroid Stimulating Hormone: Adenohypophysis secretes T.S.H. in response to ThyroidReleasing Hormone from the Hypothalamus. TSH stimulates the thyroid to secrete: Thyroxine (T4)& Triiodothyronine(T3). A. Excessive or Deficiency in production of TSH: 1. Excessive Production of TSH causes Hyperthyroidism: 2. Deficiency of TSH causes Hypothyroidism: Primary Hypothyroidism caused by Thyroid gland disorder. Secondary Hypothyroidism caused by decrease amount of TSH. B. Thyrotropin(Thytropur): is a purified extract of TSH used as a diagnostic agent to differentiate between primary and secondary hypothyroidism. Adrenocorticotrophic Hormone: Corticotropin Releasing Factor (CRF) stimulates the Pituitary corticotrophs to secrete (ACTH) secretion stimulates the release o Glucocorticoids(Cortisol) and Mineral Corticoids (Aldesterone) and Androgens from the Adrenal cortex. Usually ACTH & Cortisol secretions are in the morning versus lower in the evening , also stressors like Surgery , Sepsis, and trauma override diurnal rhythm. A. ACTH Corticotropin (Acthar) - Is used to diagnosis Adrenal disorders; treat Adrenal Insufficiency and as an anti-inflammatory drug in treatment of allergic response, if it is administered I.V. Should see in serum cortisol levels in 30-60 min. ACTH the symptoms of Multiple Sclerosis during its exacerbation phase. Pregnancy- C. Dosage: As a diagnostic test 10- 25 Units IV in 500 ml of D5W q 8 Hr. Acute MS: - Sub Q/IM 80-120 Units/day for 2-3 weeks

1. Pharmacokinestics: Absorbed well Protein Bond - Unknown a. Metabolism: t - 5-20 min. b. Excretion: Excreted in the urine. 2. Pharmacodynamics: IM Onset: 6hr. Peak: 6- 18 hrs. Duration: 12- 24 hrs. IV Onset: UK Peak: 1 hr. Duration: UK a. Side Effects: Nausea/vomiting, appetite, mood swing, Euphoria to depression, petechiae, water and Na+ retention, hypokalemia and hypocalcemia b. Adverse: Edema, ecchymosis, osteoporosis, muscle atrophy, growth retardation, depressed wound healing, cataracts, glaucoma, menstrual irregularities. c. Life Threatening: Ulcer perforation, pancreatitis. d. Drug;Food and Lab: Drug- Increase in ulcer formation with aspirin; may increase effect of potassium- wasting diuretics; decrease effects of oral antidiabetics or insulin (hypoglycemia). Posterior Pituitary Gland: Secrets Antidiuretic Hormone (Vasopressin) and Oxytocin. When there is a deficiency of ADH large amounts of water is excreted by the Kidneys Diabetes Insipidus severe fluid volume defecit. Head injuries, Brain tumors can be some of the major causes of Sudden Inappropiate Appropiate Antidiuretic Hormone secretion. ADH prepartion Vasopressin (Pitressin), Desmopressin Acetate (DDAVP) can both be administered Intravascularly or by injections. Thyroid Gland: Hormones that it secretes are Thyroxine(T4) and Triiodothyronine(T3) both are to regulate protein synthesis & energy activity . 20% of circulating T3 is secreted from the Thyroid gland and the other 80% comes from the degradation of about 40% oof the T4 . Both are carried by the blood by the Thyroxine binding globulin(TBG) and Albumin. T3 is more potent than T4 and only free unbound T3 & T4 are active and produce a hormonal response. Hypothyroidism: Synthetic T4 & T3 may be prescribed and can have either primary cause (gland disorder) or 2nd cause (lack of TSH secretion). Primary occurs more f requently T4 & TSH = Primary HypoThyroidism. The causes can be either acute or chronic inflammation of the Thyroid gland, radioiodine therapy, excessive intake of a ntithyroid drug or surgery. Myxedema is a severe Hypothyroidism- symptoms are lethargy, apathy, memory impairement, emotional changes, slow speech, deep coarse voice, edema of eyelids and face, thick dry skin, cold intolerance, slow pulse, constipation, weight gain, and abnormal menses. In children Hypothyroidism can be congenital (Cretinism). Levothyroxine Sodium( Levothyroid, Synthyroid){Prototype} - If levels of T3 and T4 ; also used to treat a simple goiter and chronic Lymphocytic Thyroiditis (Hoshimoto). To treat Hypothyroidism,Myxedema and Crentinism. Mode of action is to metabolic rate, oxygen consumption and body growth. Highly Protein Bound . Pregnancy Catergory A. Dosages- PO intially 25-50mcg/day; maintance Dose: 50-200 mcg/day. IV 0.2- 0.5 mg initially then 0.1- 0.2 mg/day until stable then go to PO doses 1. Pharmacokinestics- a. Absorption- PO 50-75% b. Distribution- PB 99% c. Metabolism- t 1/2 : 6-7 days d. Excretion- in bile and feces 2. Pharmacodynamics- PO Onset: UK Peak : 24 hr.-1 week Duration: 1- 3 weeks IV Onset: 6-8 hrs. Peak: 24-48hrs. Duration: UK

Side Effects- Nausea, vomiting,diarrhea, cramps, tremors, nervousness, insomnia, H/A, and weight loss. b. Adverse- Tachycardia, hypertension, palpitations Life Threatening- Thyroid crisis, angina pectoris, cardiac dysrhythmias, and cardiovascular collapse. Drug;Food; Labs- cardiac insufficiency with epinepherine; effects of anticoagulants, tricyclic antidepressants, vasopressors, decongestants. effects of antidiabetics (oral and insulin), digitalis, and decrease absorption with cholestyramine, colestipol. Lithyronine (Cytonel)- Synthetic T3 short t life and duration of action; not recommended for maintain therapy. It is better absorbed from GI then Levothyroid. It is used for the initial treatment of myxedema. Liotrix( Euthroid, Thyrolar)- is a mixture of Levothyroxine & Liothyronine (4:1 ratio). No advantage to using this drug over Levothyroxine alone. Hyperthyroidism: in circulating T4 & T3 which results from an overactive thyroid gland. It may be mild or severe as in Thyroid Storm. Graves Disease or Thyrotoxicosis- most common type of Hyperthyroidism caused by Hyperfunction of thyroid gland. Characterized by Tachycardia, palpitations, excessive perspiration, heat intolerance, nervousness, irritability, Exophthaalmos(bulging eyes), and weight loss. Can be treated surgically where a portion of the thyroid gland is removed(subtotal thyroidectomy) , by administering radioactive Iodine therapy, or antithyroid medications. Any of these treatments can cause Hypothyroidism. Propanolol (Beta- Adrenergic Blocker) is used to control cardiac symptoms like the tachycardia and palpitations. A. Drugs- the purpose is to reduce excessive secretion of thyroid hormones T4 & T3 by inhibiting their secretions. Thiourea Derivatives (Thioamides) - are the drugs of choice. These drugs interfere with the synthesis of thyroid hormones. They DO NOT destroy the thyroid tissue. Propylthiouracil (PTU) and Methimazole(Tapazole)- are effective thiamide antithyroid drugs. Useful for treatment for Thyrotoxic Crisis. PTU does inhibit peripheral conversions of T4 & T3. Methimazole also doesnt inhibit peripheral conversion T4 & T3 but is 10 times more potent and has a longer half life then PTU. Prolong use of thioamides may cause a goiter to form. Stron Iodine solutions Lugols solution has been used to suppress thyroid function. Sodium Iodine administered IV is useful for the management of thyrotoxic crisis. Drug Interaction Digoxin and Lithium can the action of thyroid drugs. Dilantin serum T3 levels. Parathyroid Gland- Parathyroid Hormone is secreted from this gland and is important in serum Ca+ levels. The other hormone that is important in Ca+ levels is Calcitonin this hormone serum Ca+ levels. The treatment for Hypoparathyroidism is the administration of Parathyroid Hormone. The treatment of Hyperparathyroidism is with a synthetic form of Calcitonin. A. Calcitriol (Rocaltrol) is a Vitamin D analogue that promotes Ca+ absorption from the GI

tract & secretion of Ca+ from the bone into the blood stream. Mode of action enhancement of Calcium deposits in the bone. Pregnancy Category: C Dosage: PO 0.25 mcg/day Contraindication: Hypersensitivity, hypercalcemia, hyperphosphatemia, Hypervitaminosis D, malabsorption syndrome. Caution: Cardiovascular diseases, renal calculi 1.Pharmacokinestics: a. Absorption: PO well absorbed b. Distribution: PB UK, crosses the placenta c. Metabolism: t : 3-8 hrs. d. Excretion: mostly in the feces Pharmacodynamics: PO Onset: 2-6hrs. Peak: 10-12 hrs. Duration: 3-5 days Side EffectsAnorexia, nausea, vomiting, diarrhea, cramps, drowsiness, H/A, dizziness, lethargy, and photophobia. Adverse Effects- Hypercalciuria, hyperphosphatemia, and hematuria Drug; Food; Labs- Increase cardiac dysrhythmias with Digoxin and Verapamil. Decreases calcitriol absorption with cholestyramine. Lab- Increases serum Ca+ with thiazide diuretics and calcium supplements. Adrenal Glands- 2 types of Hormones produced in the cortex : Glucocorticoids and the Mineral Corticotoids. A. Glucocorticoids(Cortisol)- is secreted from the Adrenal gland in response to the hypothalamus pituitary adrenal axis as a result of feedback. They are influenced by ATCH(Adrenalocorticoid Hormone) which is released by the anterior Pituitary gland. They affect carbohydrate, protein, and fat metabolism. Cortisol is the main Glucocorticoid is has an anti-inflamatory, anti- allergic, and anti stress effect. Indications for their use are; trauma, surgery, infections, emotional stress and anxiety. Drugs in this class are mostly a synthetic form. Conditions that they would be used for are : Mutiple Sclerosis, Rheumatiod arthritis, Myasthesia Gravis, Ulcerative Cololitis, Glomerulonephritis, shock, ocular and vascular inflammations, cerebral edema, polyarteries nosa, Hepatitis, allergic conditions, drug reactions, contact dermatitis, and anaphylaxis. Maybe used to treat organ rejections by the reciepant. Dexamethasone(Decadron)- drug used to treat severe inflammatory response resulting from head injuries or allergic reactions Prednisone(Deltasone, Orasone, Meticorten) Class is Glucocorticoid. Mode of action is to suppress inflammation and adrenal function. Also used as an immunosuppressant. Pregnancy Category- C. Adult Dose- PO 5-60 mg/day in divided doses. Contraindications- Hypersensitivity, psychosis, fungal infections. Caution- Diabetes Mellitus. Pharmacokinetics a. Absorption - absorbed from the GI tract b. Distribution- PB 65-91% crosses the placenta c. Metabolism- t - 3-4 hr. d. Excretion- In urine Pharmacodynamics- PO Onset- UK Peak- 1-2 hr. Duration- 24-36 hrs. Side EffectsNausea, diarrhea, abdominal distention, appetite, sweating, H/A, depression, flush, and mood changes. Adverse Effects/ Reactions- Petechiae, ecchymosis, hypertension, tachycardia, osteoporosis, and muscle weakness.

Life Threatening- GI hemorrhage, pancreatitis, circulatory collapse, thrombophlebitis, and embolism. Drug; Food; Labs Interactions- Drugs- effect with barbiturates, phenytoin, rifampin, ephedrine, theophylline, effects of aspirin, anticonvulsants, Ioniazid (INH), antidiabetics, and vaccines. Mineral Corticosteriods- promote Na+ retention/reabsorption and K+ excretion . They influence electrolytes, carbohydrate, protein, and fat metabolism a deficiency in them can result in a serious illness or death. A decrease in their secretion is called Adrenal Hyposecretion or Addisons disease.

Ch 32 Anti Diabetic medications

Complications from Diabetes are the 3rd leading cause of death. Ethnical groups more suspectable to Diabetes are Native Americans, Hispanics, African- Americans (2 to 3 times higher incidence) than Caucasians. Diabetes Mellitus is a disorder of the Pancreas Diabetes Insipidus- is a disorder of the Posterior Pituitary gland & Anti-Diuretic Hormone. There are 4 Forms of Diabetes: Type I Insulin- Dependent Diabetes Mellitus(Previously known as Juvenile onset Diabetes 2) Non- Insulin Dependent Diabetes Mellitus(previously known as Adult onset Diabetes)Most common occurrence of 85-90% of all diabetic cases. 3) Secondary Diabetes( due to medications such as Glucocorticoid cortisol or prednisone, thiazide diuretics like hydrochlothiazide, and epinepherine or hormonal changes) 4) Gestational Diabetes Mellitus (GDM)- during 2nd and 3rd trimesters levels of progesterone , cortisol and Human Placental Hormone increase and they can inhibit insulin usuage. There are 2 groups of Drug Therapies to treat Diabetes 1. Insulin it is a protein hormone secreted by the Beta cells in the Pancreas. They are needed for metabolism of carbohydrates, and play a role in protein and fat metabolism too. 2. Oral Hypoglycemic agents Insulin Is released from the Pancreatic Beta cells when there is an increase in serum glucose level. Normal serum glucose levels are from 70-11-mg/dl. When serum levels go above 180mg/dl then glucosuria (glucose in the urine) can occur. glucose in the blood acts as an osmotic diuretic polyuria, when blood serum glucose levels are > 200mg/dl Diabetes Mellitus occurs. Normally our bodies produce 0.2 to 0.5 units/kg/day of Insulin. Example pt weighs 154lbs which is approx. 70 kg he would produce 14-35 units of Insulin/day. Commercially prepared Insulin- Parental Insulin is obtained from either Pork or Beef . Pork Insulin is closely related to the Human Insulin, it has only one different amino acid than Humans. Therefore Pork Insulin is a weaker allergen then Beef. Beef Insulin has 4 different amino acids. Since 1983 Humulin Insulin was introduced. It has a very low incidence of causing an allergic reaction and an Insulin resistance. Subcutaneous Human (humulin) insulin is absorbed much faster and has a shorter duration than the animal insulins. This type of insulin is usually prescribed for newly diagnosed clients that are insulin dependent diabetics or in a

pregnant clients whom develop hyperglycemia and those women who are diabetics and who become pregnant. The usual dose concentration of Insulin is 100 Units/ml and is packaged in a 10 ml vial. Syringes are also calibrated to match 100Units/ml to be used for the 100U/ml Insulin type. Before using a vial of Insulin the nurse and or client must be taught not to shake the vial but to roll the vial between their palms to mix contents. Remember that Insulin is a protein and can NOT be given orally because GI secretions destroy the insulin structure! Please also remember that REGULAR Insulin is the only type of insulin that can be administered INTRAVENOUSLY! Clients should be taught a site rotation pattern to help avoid Lipodystrophy (tissue atrophy or hypertrophy) which can interfere with insulin absorption. Insulin Absorption- > when given in the Deltoid & Abdominal areas. ( the use of heat and massage will absorption). Of course illness and stress increase the need for insulin. Types of InsulinsRapid Acting- clear Include Lispro Humalog, Novolog. Onset: 5-15min Peak 30-60 min D: 3-4h Short Acting- Regular Humulin R. Onset:30-60min. Peak:2-3h D: 4-8 h Intermediate Acting- cloudy. Humulin N. Onset:1-2h Peak:4-12h D: 18-24h It may contain protamine (protein that prolongs action of or zinc that slow the onset of action and prolongs the duration of action. Long Acting- Glargine Lantus. Onset:1h Peak: None D: 24h Combination-Humulin 70/30, Novolin 70/30, Humulin 50/50. A. Oral Anti Diabetic Medications Used mostly for Type II diabetics because these clients do produce some amounts of Insulin. First group of oral diabetics were Sulfonylureas. These drugs stimulate beta cells to secrete more insulin. In the first generation of this group : Short Acting Tolbetamide Orinase Intermediate Acting- Acetohexamide (Dymelor), Tolazamide(Tolinase)

oral antidiabetic Sulfamylurea class: Amaryl, Glucotrol, Glucotrol XL used for type 2 diabetes. pancreas still producing some insulin. stimulates pancreatic beta cells to secrete insulin SE: HYPOglycemia
Long Acting- Chlorpropamide (Diabinese) 2nd generation of Sulfonylureas- the tissue response to insulin& glucose production from the liver. They have greater hypoglycemic potency, longer duration and cause fewer side effects. They should not be used in clients with liver or kidney dysfunction is present. Glimepiride (Amaryl) Glipizide (Glucotrol, Glucotrol XL) {Prototype} side effects Nausea/vomiting, diarrhea and abdominal pain. Hypoglycemia is a major side effect. Adverse: Hematological disorders aplastic anemia, leucopenia, thrombocytopenia, seizures, coma Dose- Pharmacokinetics Pharmacodynamics Biguanides (Metformin, Glucophage) acts by hepatic production of glucose from the stored glycogen, and absorption of glucose in the small intestine & it insulin receptor sensitivity. It does not cause Hypoglycemia or Hyperglycemia. It is not recommended for clients with Renal impairment. Hold for 48 hrs. before and after the client has IV contrast d/t lactic acid build up or possible development of acute renal failure. Other Anti- Diabetic Agents- Exenatide (Byetta) from amylin .Improves Betta Cell responsivenessimproves glucose control in clients with Diabetes Type II. Action is to enhance insulin secretion ; beta cell responsiveness , suppress glucagon secretion, slows gastric emptying & food intake. It is not a substitute for Insulin & should be given to patient whom have Type I Diabetes, Diabetic Ketoacidosis, some renal

dysfunction, or severe GI disease. Available in injectable pens. Promlintide Acetate(Symlin) used to improve post prandial glucose control in diabetic clients who are using Insulin but are
Ch 14 CNS stimulants and related drugs Ch 15 Antiepileptic drugs Ch 50 Acid controlling drugs Ch 51 Ch 52 Bowl disorder drugs

GERD antacid sodium bicarbonate Alka Setzer GOOD SE" constipation. Systemically absorbed .treats metabolic acidosis. can cause HYPERNatremia GERD antacid Aluminum based Amphojel GOOD SE" constipation. Binds phosphate, used w/renal pts. to focally eliminate phosphorus GERD antacid calium based Calcium carbonate Tums GOOD SE: constipation. tms used to increase calcium for osteoporosis and in renal pts. BEWARE w/HYPERglycemia

antidiarrheals Immodium(OTC) Lomotil (prescription) for treating diarrhea decreasing peristalsis. assessment of hyperactive bowel sounds. important due to loss of fluid and electrolyte imbalances. try Gatorade and pedialyte. MD may want to test for culture and O&P=test for worms. Chemically related to OPIATES assess for ALLERGIES Lomotil/Immodium (prescript/OTC) used to treat diarrhea chemically related to opiate so assess for allergy
Antiemetic and anti Nausea Ch 53 Vitamins and minerals Ch 54 Nutritional supplements

PHARMACOLOGY STUDY GUIDE 5 rights of medication administration

1. right PT 2.right ROUTE 3.right DOSE 4. right Time 5. right Medication

Cummulative Section Pharmacology: The study of drugs and their interactions with living systems Encompasses the study of the physical and chemical properties of drugs as well as their biochemical and physiological effects. Clinical Pharmacology: Study of drugs in humans (includes study of drugs in patients as well as healthy volunteers). DRUGS: Effectiveness: Most important! Elicits the response for which the drug is given. Current US law requires proof effectiveness prior to release for marketing. Safety: One that cannot produce harmful effects (there is no such thing as a SAFE drug) Selectivity: Elicits only the response for which it is given thus no side effects (No such thing as a selective drug). Pharmacotherapeutics: The medical use of drugs (use to dx, prevent or treat disease, or prevent pregnancy) Pharmacokinetics: The study of the movement of drugs through the body. Four Basic Processes 1. Absorption (think stomach) 2. Distrubution (think blood flow) 3. Metabolism (think liver) 4. Excretion (think kidney) Process is determined by the concentration of a drug at the site of action determines intensity and time course of responses. Movement through the body: drugs must cross membranes, most commonly by dissolving directly into the lipid bilayer of the membrane to cross (lipid soluble drugs can cross membranes, but polar or ionized cannot). Other pathways to cross membranes: 1) passing through the pores 2) undergoing transport 3) penetrating membrane directly (common) Absorption: the movement of a drug from its site of administration into the blood. -Enhanced absorption occurs by rapid drug dissolution, high lipid solubility, a large surface area, and high blood flow at the site of administration. Distribution: defined as the movement of drugs throughout the body. - In most tissues, drugs can easily leave the vasculature through spaces between the cells that compose the capillary wall. - Many drugs reversibly bind to albumin. While bound to albumin, drug molecules cannot leave the vascular system.

Metabolism: Biotransformation. Enzymatic alteration of drug struction -most takes place in the liver and is catalyzed by cytochrome p450 system of enzymes. -Most important consequence of drug metabolism is promotion of renal drug excretion Excretion: Most drugs are excreted by the kidney. -Renal drug exretion has 3-steps: glomerular filtration, passive tubular reabsortion, and active tubular secretion. -Drugs that are highly lipid soluble cannot be reabsorbed back into the kidney -Drugs can be excreted into breast milk. First-Pass Effect: rapid inactivation of some oral drugs as they pass through the liver after being absorbed. Essentially, how much drug is left available after passing through the liver. Used to determine dosage and intensity. Bioavailabilty: free-circulating drug system (post-first pass) even after binding. Half-Life: Time required for the amount of drug in the body to decline by 50%. Shorter the half-life, the more frequent the administration. Time to reach plateau about 4 half-lives. Drugs with a long half-life may need a loading dose to reach plateau. Pharmacokincetic tolerance: results from a accelerated drug metabolism. Pharmacodynamics: What drugs do to the body. The study of biochemical and physiologic effects of drugs and molecular mechanisms by which those drugs are produce. Reducing risk of adverse interactions: minimize # of drugs the patient is on. Take a thorough drug history. Adjust dosages when using an inducing agent. Adjust timing of administration to reduce absorption problems. Monitor for early signs of toxicity. Be vigilant when a patient is on a drug with a low therapeutic index. Pharmacodynamic tolerance: results from adaptive changes that occur in response to prolonged exposure. It increases the MEC of a drug. Allergic Drug Reaction: an immune response. Estimated <10% of adverse reaction are allergice type. Intensity of reaction is dependent on degree of immune sensitization not dose size. Medication Errors: Any preventable event that may cause or lead to inappropriate medication use or patient harm, while the medication is in the control of the healthcare professional, patient, or consumer Medication Errors: Major cause of morbidity and mortality. Can be made by many people, incuding pharmaceutic workers, pharmacists, physicians, transcriptionists,

is

nurses, patients and patients families. 3 Common types of Fatal Med Errors: Human factor, Miscommunication, Confusion caused by similarities in drug names. (Others include packaging, formulations, delivery devices, labeling and reference materials). Effective measures for reducing med Errors: using safety checklist for high alert drugs. Replacing handwritten med orders with computerized order entry system. Having a clinical pharmacist accompany ICU docs on rounds. Avoid error-prone abbreviations. Use a computer bar-code system. Therapeutic Index: (LD50: ED50) A measure of a drugs safety. Drugs with a high TI are presumably safe. FDA Drug Approval Process: Preclinical testing (in anmials) Toxicity Pharmacokinetics Possible Useful effects | Investigational New Drug (IND) Status | Clinical Testing (in humans) Phase I subjects: normal volunteers ; tests: metabolism and biologic effects | Phase II subjects: patients ; tests: therapeutic utility and dosage range | Phase III subjects: patients ; tests: safety and effectiveness | Conditional Approval of New Drug Application (NDA) | Phase IV: postmarketing Surveillance Beta1=heart Beta2=lungs

anticholinergic atropine dries you up, ups heart rate,slows diarrhea, contraindicated in:glaucoma and GI disorders. Monitor VS and HR, monitor constipation,oliguria.Take 30 min before food. eat high

fiber and lots fluids Demerol narcotic NO anti-cough properties, used during labor, sort term use only!!! Used often for procedural sedation along w/other drugs such as Versed. No intubation necessary. airway is protected. SE: not for the elderly because of te breakdown in teir bodies. can cause SEIZURES, irritability, agitation 1st pass goes to liver

direct acting muscle relaxant Dantrium Potent muscle spasm relaxer, direct effect on muscle.LONG term use . 8 weeks. used for MS, and spinal cord injury also used to treat malignant hyperthermia. POTENTIAL LIVER toxicity-hepatoxic R/T anesthesia

Demerol can cause seizures used in OB short term use digoxin level 0.5-2

antagonist stops something from happening sulfonamides 1. Bactrim 2. Septra 3. Silvadene cream used to treat UTI, baby eye prophalaxis, chlamidia, pneumocytis, carinii pneumonia, absorbed by GI tract. po, IV. LABS: CBC & creatinine. check for allergies. check I/O's. Push fluids. AVOID last 2 months of PREGNANCY!!! SE: Steven Johnson SYNDROME, crystalluria, photosensitivity. 1. Treats UTI 3.treats burns flu/herpes (antiviral) Symmetrel (antiparkinson) treats Influenza A used w/ELDERLY SE: ORTHOHYPOtension Loop Diuretic Lasix inhibits reabsoption of Na, promotes urine output. lose Na,Cl,H2O,Magnessium and Potassium. ok for Renal pts. for edema w/CHF, cirrhosis or renal failure, fuorosemide for HTN. Chemicall related to SULFA SSESS for ALLERGY. give SLOWLY 20mg/mn or can cause permanent transient hearing loss! Everything DERCEASES except GLUCOSE and URIC ACID rises. daily wt., monitor for Digoxin toxicity. Teach high Potassium! RAAS System renin angiotension aldesterone system If pt. has low BP=RAAS is sensed=kidneys release renin, liver produces angiotensin1converts to angiotensen 2 by ACE=then adrenal glands secrete aldosterone(the sodium saver, which saves h2O) pituitary gland secretes ADH(no pee hormone) this helps body retain fluid=re-establishes BP!

PPI PREVACID PROTONIX NEXIUM give 1st thing in the morning best for GERD Narcotic Dilaudid 7-10 x's more potent than Demerol. Shorter acting than Morphine

SE: drowsiness no alcohol

decongestant Sudafed congestion secondary to dilation of nasal blood vessels. stimulates alpha receptors and shrinks the mucous membranes and reduces fluid secretion(runny nose)STOPS MUCOUS! SE: restless, tremors, elevated BP, elevated Glucose. nasal spray overuse can cause rebound nasal congestion. BEWARE w/HTN or cardiac hx in pts. CAN cause MI, stroke due to elevated BP. also use for "stuffy ear" in airplane pain Prostoglandin analogue (synthetic) Cytotec cytoprotective.for pts taking NSAIDS potassium 3.5-5.3 give w/full glass of H2O NEVER PUSH!!!! dilute invert IV bag can do IVPB Diuretics make levels LOW "reg" insulin onset 30 min before eating meal

cholinergic reglan vessels dilate, lowers HR, ups peristalsis, ups salivation. prevvents constipation. side effect: distonic reaction Ritalin to treat ADHD CNS stimulant give in morning anti-lipemics(lipid lowering) "statins" HDL>60 and LDL ,100 total ,200 inhibits HmG-CoA reductase-enzyme that produces LDL at night. TAKE at BEDTIME except LIPITOR. Cholesterol affects LIVER so assess CPK, AST, ALT. shrinks plaque to prevent stroke .has anti-inflammatory effects so may help COLON CANCER and ALZHEIMERS. SE: myalgia, rhabdomyolysis. NO grapefruit juice. LOW fat DIET UTI med Pyridium/analgesic relieves pain, burning sensation, and frequency and urgency. blood test to monitor

glucose levels. monitor for GI disturbances, HEMOLYTIC ANEMIA, NEPHROtoxicity, and HEPAtoxicity. SE: HEMOLYTIC ANEMIA, NEPHROtoxicity, HEPAtoxicity, urine will become redish orange colored SNS epinephrine Adrenaline Beta1=heart Beta2=lungs UTI meds macrodantin E. coli Tx of acute and chronic UTIs. CBC w/long term therapy... assess RENAL and HEPATIC function. monitor output and obtain culture before therapy....SE: anorexia, n.v, discoloration of urine, superinfection, HEPAtoxicity deltoid inj (IM) 1 ml of medication landmark: acromian process opiate w/narcan used to treat pain and prevent narcotic addiction Heparin subcut or IV used for prophylaxis or acute events. Prolongs clotting time. Labs: PTT(1.5-2.5) ANTIDOTE: Protamine Sulfate...assess for bleeding, use soft toothbrush, electric shaver. WBC range 4-10,000 Beta Blockers "OLOLS" Inderal(non-selective) all others selective. decreases contractibility in heart, lowers renin release in KIDNEYS, and sympathetic output. for HTN,angina,MI,dysrhthmias.SE=BRADYcardia,hyPOtension,bronch constriction,lowers blood sugar.Hold for BP less than 60 or systolic less than 90. Inderal can decrease test anxiety antitussive narcotic: CODEINE over the counter: DEXTROMETHORPHAN suppresses cough reflex. if cough is nonproductive and irritating:can give antitussive. productive cough may be useful. GIVE AFTER MEALS!!!! oral antidiabetic Biguanide class : Glucophage decreases hepatic production of glucose, increases insulin receptor sensitivity.May be combined with other hypoglycemia needs. WITHHOLD 48hrs before and after tests using IV contrast dye;LACTIC ACIDOSIS and RENAL FAILURE may DEVELOP!!!! LIVER NSAID aspirin(ASA) falls under multiple classes analgesic,antipyretic,antiplatelet,anti-inflammatory,menstrual pain. Check for ASA allergies.assess hx for GI upset,bleeding & lier disease. TAKE with FOOD or FULL glass of WATER. admin PPI to reduce risk of ulcr. SE: no PREGGOS LAST TRImester,n

alcohol,don't take w/other NSAIDS,kids with flu like sx cant tae(reye's syndrome) SE: GI upset, bleeding,renal failure, TINNITUS insulin injection subcut into fatty tissue abdomen the best orange insulin syringe only anticholinergic atropine dries you up, ups heart rate,slows diarrhea, contraindicated in:glaucoma and GI disorders. Monitor VS and HR, monitor constipation,oliguria.Take 30 min before food. eat high fiber and lots fluids IV heparin drip know PTT lab (2-4) if too high=bleeding if too low=clot check PTT every 6hrs heparin 90 degree inj DONT aspirate 2 inches away from umbilicus narcotic Demerol NO anti-cough properties, used during labor, sort term use only!!! Used often for procedural sedation along w/other drugs such as Versed. No intubation necessary. airway is protected. SE: not for the elderly because of te breakdown in teir bodies. can cause SEIZURES, irritability, agitation. 5 rights of medication administration 1. right PT 2.right ROUTE 3.right DOSE 4. right Time 5. right Medication 1st pass goes to liver flu/herpes (antiviral) Valtrax used to treat/prevent herpes take daily po bid to prevent herpes break out bulk forming laxative : natural fiber Fibercon, citrucel,Metamucil large soft stool. Mix at bedside, drink immediately, follow with glass of water calcium channel blockers Calan,ProCardia,Cardizem lowers myocardial contraction and eases workload,lowers HR and BP, raises blood flow to heart, lowers peripheral vasorestiction for HTN, angina, A-fib,migraines SE=HYPOtension,HA, "blah" feeling....monitor hepatic and renal function, assess BP and HR direct acting muscle relaxant Dantrium Potent muscle spasm relaxer, direct effect on muscle.LONG term use . 8 weeks. used for MS, and spinal cord injury also used to treat malignant hyperthermia. POTENTIAL LIVER toxicity-hepatoxic R/T anesthesia (2nd generation NSAID) cox 2 inhibitor Celebrex TX of osteoarthritis & rheumatoid arthritis,menstrual discomfort.LONG TERM use. assess for HX of RENAL or HEPATIC dysfunction,HYPERtension,fluid retention, heart

failure, infection, GI bleeding or ulceration, concurrent anticoagulant therapy,steroids, or alcohol use. INCREASE FLUID intake.monitor RENAL function. SE: HA,sinnusitis,flatulence,peripheral edema, GI upset/bleed Coumadin PO inhibits hepatic synthesis of VIT k dependent factors.Use for chronic A-Fib, prosthetic heart valves, CHRONIC anticoagulation needs:prevents or slows the action of blood clots.LABS:PT & INR(2-3) ANTIDOTE:Vit K.SE: anorexia, bleeding, heamaturia, thrombocytopenia, hemmorrhage. assess for bleeding-stools & GI. AVOID foods rich in VIT K(leefy greens)no ASA and NSAIDS preventative anti inflammatory Flovent Singulair(inflammation to lungs) inhaled corticosteroid:take daily.rinse mouth after using to prevent thrush. NSAID inhaler for prevention. effective in reducing inflammatory symptoms of asthma triggered by allergic and environmental stimuli.these groups recommended for acute asthma attacks eyedrop admin from inner to outer in conjunctival sac press on duct for a bit to prevent systemic absorption potassium level 3.5-5.3 GERD antacid sodium bicarbonate Alka Setzer GOOD SE" constipation.Systemically absorbed. treats metabolic acidosis.can cause HYPERNatremia multi lumen cath central line short term HIV AZT given to pregnant HIV mothers to prevent passage of disease also given prophalaxic after needle stick CNS depressants benzodiazepines "lam & pam" Temazepam used to treat insomnia & to decrease nocturnal awakenings short term use GIve at BEDTIME check for signs of repiratory distress. AVOID ALCOHOL & other CNS depressants SE: hangover, light-headedness, dizziness, or confussion overdose: administer an EMETIC and follow w/activated charcoal/conscious pt or gastric lavage/unconscious pt administer ROMAZICON has sedative effect 3 check of medication administration 1. when taking med out of cabinet 2.after you have taken out all medication and put the drawer back 3. at bedside before you give pt the med oral antidiabetic Sulfamylurea class: Amaryl, Glucotrol,Glucotrol XL used for type 2 diabetes. pancreas still producing some insulin.stimulates pancreatic bta cells to secrete insulin SE: HYPOglycemia

macroglides 1. erythromycin PCN SUBSTITUTE TX of respiratory infections,skin infections,babies eyes LAB: liver enzymes(AST 0-35 & ALT 4-36)send sample to lab GIVE w/full glass of H2O IV:dilute,infuse SLOWLY NEVER IM (too painful) Low dose:bacteriostatic High dose" bacteriocidal SE: HEPAtoxicity, GI disturbances Hemoglobin 12.6-17.4 inhaler shake 1st wait 1 min between puffs rinse mouth after steroid inhaler Leukotriene agonist MONTELUKAST ZAFIRLUKAST therapeutic range 10-20 antidiarrheals Immodium(OTC) Lomotil(prescroption) for treating diarrhea decreasing peristalsis.assessment of hyperactive bowel sounds. important due to loss of fluid and electrolyte imbalances. try gatorade and pedialyte.MD may want to test for culture and O&P=test for worms. Chemically related to OPIATES assess for ALLERGIES! aminoglycosides "mycin" gentamycin neomycin sreptomycin gram-for serious infections IM>IV,except neomycin(po) neomycin decreases ammonia level. assess VS,urine output. MAY DECREASE K+ & Mg+ renal & hearing baseline.check for neurotoxicity & ototoxicity LABS: BUN,creatinine. IV dilute & infuse 30-60 mins.culture before & after starting therapy monitor I/O's, hearing,labs. PUSH FLUIDS peak &thru levels(narrow TI) SE: NEPHROtoxicity,OTOtoxicity Isotonic solution NS & LR NS & LR used for dehydration antifungals "zole"drugs amphotericin yeast,fungal pneumonia,ringworm,jock itch,athlete's foot AMPHOTERRIBLE: IV SLOWLY only, life threatening fungal infections LABS: liver enzymes(NEPHRtoxic)BUN, creatinine,bilirubin protect from light NO ALCOHOL be careful of thromophlebitis at IV site SE: shake & bake(fevers/chills) *****premedicate w/tylenol & benadryl*** demerol can cause seizures used in OB short term use ao both ears digoxin level 0.5-2 anti-gout Allopurinol low serum uric acid levels, prevents attacks. assess uric acid levels, CBC,uric acid foods:wine,alcohol,organ meats,sardines, salmon,gravy. check I/O's, increase fluid,take AFTER MEALS, yearly eye exams. "disease of kings""unwalkable disease" inflammation condition,attacks joints & tendons. Caused by excess uric acid . SE: pruritus, metallic taste, GI upset/bleed,malaise H2 blockers Tagamet Zantac Pepcid Axid BETTER histamine receptors antagonist .used to prevent and treat ulcers and GERD. decreases gastric acid secretion by inhibitingH2 receptors in stomach.take PRIOR to MEAl and at

bedtime. SE: HA,dizziness,constipation,skin rash,gynecomastia(enlrged breast in male)stop drug and it goes away, impotence(reversible) Lomotil/Immodium (prescript/OTC) used to treat diarrhea chemically related to opiate so assess for allergy Antihistamine(H1 blockers) Benadryl (newer: Claritin, ALLEGRA(more specific) compete for hystamine receptor site to decrease nasopharyngeal secretions. have anticholinergic properties:(urinary retention, dry secretions,dry mouth). CAUTION with BPH and GLAUCOMA. SE: drowsiness..for acute asthmatic attack, respiratory;also allergic reactions, prevents motion sickness, sleep aid and antitussive. depress CNS DONT take with ALCOHOL, narcotics Use BEFORE allergy onset. SE:ARRYTHMIAS, sedationthick secretions...ALWAYS assess pt for urinary retention PRIOR to starting therapy GERD antacid Aluminum based Amphojel GOOD SE" constipation. Binds phosphate, used w/renal pts. to focally eliminate phosphorus antimalarials Aralen prophylaxis(before,during,after trip) S & SX: fevers,chills,sweats. assess hearing & visual changes. take W/FOOD Avoid alcohol caused by parasitic protozoal destroys RBC, impairs O@ delivery SE"GI upset, cranial nerve 8(hearing) involvement, renal impairment Cox 2 inhibitor Celebrex used for osteoarthritis SE:GI upset central line push pause method flu/herpes (antivirals) Tamiflu take w/in 48 hrs of onset flu shot inactive nasal is live virus(live virus not for young,preggo,or immunocompromised) flu shot yearly unless ALLERGIC to EGGS of HX of GUILLIANE-BARRE IV:slow lots of H2O SE: NEPHROtoxicity,OTOtoxicity central acting muscle relaxants SOMA Flexeril Skelaxin used for muscle spasms, diseases, involuntary motor activity. Depresses CNS. SE: drowsiness, NO ALCOHOL!taper off dont stop abruptly.SHORT term 3 weeks or less. Take w/ food BUN / creatinine 10-20 / 0.5-1.2 corticostreoids PREDNISONE to decrease inflammation.cortisone can get shots. DEXAMETHASONE: for inflammation of the brain.used for inflammation conditions(autoimmune disorders),allergy, prevents organ rejections. Monitor: VS, BP, wt., blood glucose, electrolytes, ECG cushing-like symptoms...buffalo hump, sodium elimination SE" HA,HYPERglycemia, increase in BP, HR, appetite. not healing quickly.GI upset.ups SODIUM and GLUCOSe...lowers Potassium and Calcium. SE: muscle wasting,mood changes, demineralization of bones. tetracycline DOXYCYCLINE BROAD spectrum,bacteriostatic po/IV, NEVER IM(too painful)txs acne & tick-born illness LABS: BUN,creatinine, culture before starting therapy. TAKE on EMPTY STOMACH NO MILK(admin 1 hr ac & 2hr pc) NO ANTACIDS NO PREGGOS because pills less effective SE: photosensitivity,tertogenic,gray teeth,NEPHROtoxicity

ad right ear "statin" meds given for high cholesterol change diet exercise REPORT CRAMPS TO DR LABS: AST/ALT 0-35,4-36 give at NITE except LIPITOR IN MORNING antagonist stops something from happening adult ear pull up and back sulfonamides 1. Bactrim 2. Septra 3. Silvadene cream used to treat UTI,baby eye prophalaxis,chlamidia,pneumocytis,carinii pneumonia, absorbed by GI tract. po, IV. LABS: CBC & creatinine. check for allergies.check I/O's.Push fluids. AVOID last 2 months of PREGNANCY!!! SE: Steven Johnson SYNDROME, crystalluria,photosensitivity. 1. Treats UTI 3.treats burns tetracycline NO DAIRY!!!! NO PREGGOS!!!!! can cause grey teeth so NO KIDS!!! flu/herpes (antiviral) Symmetrel(antiparkinson) treats Influenza A used w/ELDERLY SE: ORTHoHYPOtension RBC range 4.2-6.1 million fluoroquinolones ciprofloxacin levofloxacin gatifloxacin BROAD spectrum.interfers w/the enzyme DNA gyrase. treats anthrax,UTI,resp. infection, skin infection. LABS: BUN,creatinine. increase fluid intake NO PREGGOS monitor I/O's antacid & iron lower absorption SE: nausea,vomiting,diarrhea,ARCHILLES tendon rupture,tinnitus Loop Diuretic Lasix inhibits reabsoption of Na,promotes urine output.lose Na,Cl,H2O,Magnessium and Potassium.ok for Renal pts.for edema w/CHF, cirrhosis or renal failure, fuorosemide for HTN.Chemicall related to SULFA SSESS for ALLERGY.give SLOWLY 20mg/mn or can cause permanent transient hearing loss!Everything DERCEASES except GLUCOSE and URIC ACID rises. daily wt., monitor for Digoxin toxicity.Teach high Potassium! RAAS System renin angiotension aldesterone system If pt. has low BP=RAAS is sensed=kidneys release renin,liver produces angiotensin1converts to angiotensen 2 by ACE=then adrenal glands secrete aldosterone(the sodium saver,which saves h2O) pituitary gland secretes ADH(no pee hormone) this helps body retain fluid=re-establishes BP! antitubicular Isoniazid (INH) give if they have been exposed treats TB prophylaxis AFB isolation negative pressure prevent peripheral neuropathyw/vitamin B6 (pyridoxine)(INH) collect early am sputum for acid fast bacillus X3 S &sx:night sweats,fever,productive cough give 1h ac or 2h pc DOTS tx: directly observed tx eye exams NO ANTACIDS!!! SE: HEPAtoxic, jaundice NSAID Toradol analgesic.INTRAOCULAR anti-inflammatory. monitor RENAL/HEPATIC function.observe client for signs of bleeding. SHORT term use for pain.OPTHALMICrelieve itching caused by allergic conjunctivitis. SE: HA,nausea,peptic ulcer,hepatic reaction,nephrotoxicity in pts. w/preexisting renal impairment

PPI PREVACID PROTONIX NEXIUM give 1st thing in the morning best for GERD ratio 1:100 1 gram in 100 ml acetaminophen: tylenol, excedrin, goody's, midol fever,pain,HA monitor HEPAtoxicity AST 0-35 ALT 4-36, pain check for jaundice and bleeding ANTIDOTE: mucomyst causes little to no GI disturbances Narcotic Dilaudid 7-10 x's more potent than Demerol.Shorter acting than Morphine SE:drowsiness no alcohol Lipid IV solution can hang 12 hrs TPN IV solution mixture good for 24 hrs can hang for 4 hrs methylxanthine class Theo dur Pts. with COPD. acts like caffeine.stimulates SNS:bronchodilation.smooth muscle relaxant of respiratory system:opens airways.used for asthma, COPD. Stimulates CNS, leads to diuresis, tremors,dysrthmias.narrow therapeutic(10-20mcg)monitor serum level.give IV slowly!smoking increases metabolismof drug:smokers need higher doses. ASSEESS lungs! maintain hydration, avoid caffeine!assess cardiac and CNS response(dysrythmias, HTN,tremors) Ace inhibitors "prils" used to treat HTN.doesnt let angiotensin 1 convert to angiotensin2.lowers BP with no effect on HR.used with DM and HTN.prevents stroke, MI due to inflammation.used for renal protection=lowers pressure in glomerus;protects the kidneys.Can lead to HYPERKalemia.Angiotensin 2 Bad cause it increases inflammation, clots and resistant to insulin.SE=cough, HYPERKalemia. Assess: BP, urine protein, BUN/CREAT, CBC,K, and Na levels. COUGH, HYPOtension, HYPERKalemia, may lose taste for food.NOT for RENAL "log" insulin works w/in 15 min so have food ready to give phosphate level 1.8-2.6 "pril" meds do nothing to pulse but lower BP hyperKalemia and cough magnesium level 1.2-2.5 cardiovascular Digoxin pos. inotrop neg. chronotope Increases force of contraction and decreases HR.for heart failure and dysrhthmias.narrow therapeutic(0.5-2)hold for Bp less than 60.monitor for BRADYCARDIA,halos around lights.HyPOKalemia cause more risk for toxicity cause as potassium drops the cardiac muscles sensitivity increases.RENAL impairment because KIDNEYS cant excrete digoxin.watch BUN/CREAT antidote:digibind.EAT high POTASSIUM!! decongestant Sudafed congestion secondary to dilation of nasal blood vessels. stimulates alpha receptors and shrinks the mucous membranes and reduces fluid secretion(runny nose)STOPS

MUCOUS! SE: restless,tremors, elevated BP,elevated Glucose.nasal spray overuse can cause rebound nasal congestion. BEWARE w/HTN or cardiac hx in pts. CAN cause MI, stroke due to elevated BP. also use for "stuffy ear" in airplane pain. Prostoglandin analogue (synthetic) Cytotec cytoprotective.for pts taking NSAIDS potassium 3.5-5.3 give w/full glass of H2O NEVER PUSH!!!! dilute invert IV bag can do IVPB Diuretics make levels LOW low molecular weight heparin....Lovenox used to prevent DVT for post-op, prevents acute event, lowers risk of bleeding.HIGH ALERT DRUG!!! SE: fever, confusion,nausea, thrombocytopenia,bleeding.DONT MIX WITH OTHER DRUGS=increase risk of blleding...ASSESS for bleeding. SUBCUT ONLY.Teach soft toothbrush.leave bubble in syringe.LOVE handles calcium level 4.5-5.5 "reg" insulin onset 30 min before eating meal GERD antacid calium based Calcium carbonate Tums GOOD SE: constipation. tms used to increase calcium for osteoporosis and in renal pts. BEWARE w/HYPERglycemia. antitubercular Rifampin (if active TB) treats active TB collect early am sputum for acid fast bacillus X3 S &sx:night sweats,fever,productive cough give 1h ac or 2h pc DOTS tx: directly observed tx SE: brown rust discolor HIV antiviral zidovudine (AZT) wont allow RNA to convert to DNA treats HIV(decrease maternal transmission) SE: neutopenia,bone marrow suppression, anemia, neurological problems,confusion HIV antiviral RETROVIR prophlaxis for accidental needle sticks SE: LOW EVERYTHING....HYPOtension,HYPOglycemia enteric med digested in small intestine LABA long acting beta agonist SEREVENT long term use. broncho dialation.slow onset but long duration.. NOT for ACUTE attacks.decreases resp. tract edema.watch for thrush so wash mouth after use. Use bronchodilator 1st.taper off gradually.for ASTHMA control asthma preventative med ATROPINE SABA-Atrovent LABA-Spiriva anticholinergic inhalerwhich allows SNS to dominate. bronchodilation. Dries you up. narcan antidote for narcotic toxicity CNS depressant nonbenzodiazepine Zolpidem (Ambien) to treat insomnia SE: drowsiness,lethargy hangover,irritability,dizziness,anxiety anti-gout/inflammatory COLCHINE Tx of acute gout & prophylaxis of recurrent gouty arthritis. Assess medical HX for any gastric,renal(SUFFICIENT RENAL function needed),cardiac or liver disorders. assess serum uric acid & urine output. monitor urine output & watch for possible kydney stones.

SE: pruritus, metallic taste, GI upset/bleed GOUT colchine for pain Allopurinol to treat NO alcohol No organ meats low protein diet ventro gluteal inj (IM) 3 ml of med landmarks: greater trochanter and ileac spine Vancomycin Oto & NEPHRO toxic used to treat MRSA dilute and infuse over 1 hr if given to fast can cause REDMAN syndrome cephalosporine-"cef/ceph" cephalexin cefadroxil cefaclor resistance to penicillinase. assesss for allergies to penicillin because may be allergic to cef. LABS: BUN,creatinine. monitor VS,I/O's. culture before & after therapy. SE: Nauesea,vomiting,diarrhea, NEPHROtoxicity,increased bleeding Thiazide diuretic know if allergy to sulfa loose potassium so give high potassium diet bananas kid ear down and back Coumadin Vit K is antidote lab: INR(2-3 is therapeutic) want PT & INR high GERD antacid magnessium based Maalox Mylanta GOOD SE: diarrhea. maalox combines w/broth magnesium & aluminum toconteract diarrhea & constipation. aniemetics 1.Dramamine/2.ANTIVERT(non prescription) 3.VISTARIL9antihistamine) 4.Transderm-scopanticholinergic) 5.Phenergan(phenothiazine) 1. for motion sickness,take 30 min prior to travel.2. used for vertigo 3. dries you up SE:drowsiness 4. behind ear patch great for motion sickness. lasts 3 days/SE: urinary retention. 5. inhibits CTZ in medulla.potent works in brain. sedative effect:promotes drowsiness. urinary retention and constipation. BEWARE of distonic reaction! IV: destroys tissue if given too fast.MUST be diluted and given slowly!!!monitor bowel sounds and electrolytes. assess urinalysis prior and during. Helicobacter Pylori(H-pylori) combination ; Flagyl,Biaxin,Prilosec triple therapy treatment.. linked to PUD when ulcer not caused by NSAIDS. Noninvasive breath test can detect. NSAID ibuprofen (motrin,advil,nuprin,medipren) analgesic,anti-inflammatory,antipyretic. Check for allergies.check hx for severe RENAL or LIVER disease,peptic ulcer, or bleeding disorder,GI upset, or peripheral edema. Take with full GLASS of WATER. observe for BLEEDING GUMS, black stools, GI discomfort. SE: NEPHROTOXICITY, Tinnitus,GI bleeding chloride level 95-108 hypotonic soultion 0.45% NS dialysis pt or diabetic patient with ketoacidosis Carafate coats ulcer to prevent acid from doing further damage Dilantin used to treat epilepsy narrow therapeutic range if too high dont give if too low look for

dose to be raised can cause gingival hyperplasia ou both eyes dilantin and theophylline levels 10-20 Vastus lateralis inj (IM) 3 ml of med landmark:greater trochanter Loop diuretic LASIX lasts 6hrs gets rid of sodium & potassium IV 20mg/mn must have adequate renal function daily wt I/O give high potassium diet bananas given to pts w/ACUTE pulmonary edema Narcotic Morphine Mod-severe pain, depresses resp & cough. check for Hypotension monitor VS,output,bowels sounds, assess allergies,resp.,12 or systolic,90 withold SE: CO2 retention, pupillary CONSTRICTION,VASdilation,nausea/vomiting, ortho HYPOtension,pruitis. Decrease peristalsis=Constipation& urine retention, NEUROtoxicity ANTIDOTE: NARCAN Thiazide diuretic HCTZ Chemically realed to SULFA assess for ALLERGY!lose Na,Cl,H2o, and K,increases calcium, glucose, and uric acid. used for HTN and edema associated with CHF. PT. MUST HAVE NORMAL renal function.Caution w/Diabetics! SE: HYPOkalemia, caution w/elderly, diabetics, gout. TEACH HIGH POTASSIUM!!!assess for Digoxin toxicity hyperglycemia sx sweating,confusion narcotic agonist-antagonist Talwin Control mod-severepain. Obtain drug hx,baseline VS. Monnitor VS, bowel sounds, I/O SE: HYPOtension, constipation what do you give at 1st sign of chest pain if no nitrates? ASA 325mg chew it up and call 911 anti-lipemics TRIGLYCERIDE 1.RELIANT 2. Zetia 1.prescription strenght fish oil to lower fatty liver. EAt fish or 1000mg of fish oil. 2. lowers triglycerides by inhibiting cholesterol absorption, usually combined with "statin". (Zetia+"STATIN=Vytorin) obesity:causes too much fatin liver=high cholesterol(LDH)==BAD!!!! antacids dont give with medications!` CNS stimulant Ritalin to correct hyperactivity caused by ADHD, increase attention span, treat fatigue, and control narcolepsy. determine if hx of heart disease,HYPERtension,HYPERTHYROIDism,parkinsonism,or glaucoma. labs:CBC,WBC,platelets before and during therapy. give morning & lunch. Avoid alcohol & caffeine. monitor weight. SE: HA,nausea,diarrhea,nervousness SABA short acting beta 2 agonist Albuterol XOPENEX fast acting rescue inhaler.bronchodilation:opens up airways,decreases airway resistance.for asthma,bronchitis,emphysema. SE: nervousness, tremors, TACHYcardia, irregular HR, HTN, dysrhthmias.Assess: lung sounds,VS(HR and BP may inncrease).

teach correct use of inhaler.carry at all times.Xopenex is hand held treatment nebulizer trough of med draw 30 min before next dose of med is due Magnesium can cause diarrhea Phenergan for nausea very toxic so IV DILUTE & push SLOWLY ani-anemics iron (FE) hemoglobin regeneration treats anemia Hgb lab bleeding out somewhere INJ:z-track method Liquid:drink thru straw(so not to discolor teeth) drinks lots of H2O Vit C INCREASES absorption Pt. could need blood transfussion and O2 therapy iron foods: spinach,fruit,veg, egg yolks SE: black/green stool,constipation emollients/lubricants: stool softeners Surfak Colace Mylicon(adults) lubricates to prevent constipation.used with narcotics, after surgery, after MI, no straining. SIMETHICONE-anti gas ONLY(babies) PTT (heparin) therapeutic range for person on HEPARIN 2-3 AST/ALT 0-35 / 4-36 osmotic laxatives Go LYtely(isotonic w/electrolytes added) hyperosmolar salts pull H2O into colon, increases bulk and perostalsis. used for bowel prep.3-4 liters over 3 hrs. best when cold. want to be clear of stool prior to colonostomy.cleans you out.SE: abdominal cramping, diarrhea.results in loose,watery stool. lidocaine 2% 2 grams in 100 ml TB injection intra dermal bevel up look for wheel 48-72hr check 15 mm (induration) indicates pos adrenergic blockers-Beta Blockers "olol" Propanolol(non-sel) Metoprolol(sel) treats cardiac dysrythmias ,mild GYPERtension,mild TACHYcardia,angina pectoris, Extreme caution w/COPD & asthma decreases HR and BP SE: BRADYcardia Metaprolol safe for resp, patients Plavix ANTIPLATELET Tto prevent MI/stroke SE: bleeding potassium SPARRING diuretics Aldesterone(Aldactone) promote NA and H2O excretion;but retain Potassium.SE: HYPERKalemia.Pt. MUST HAVE adequate RENAL function! Assess K levels. Use for LONG TERM control of fluid volume excess with cirrhosis of liver. AVOID salt substitutes!(HIGH in Potassium) daily wt. peek of a med draw 30-60 after med is given anticonvulsant Dilantin used to prevent grand mal & complex partial seizures stop seizures w/IV valium or IV ativan BUN ,creatinine IV w/NS only monitor serum drug levels (10-20) Good ORAl care SE: anorexia, diplopia, ataxia,slurred speech, HYPOtension,pink-red/brown discoloration of urine, increased glucose levels for diabetics, reduce platelets

Benzodiazepine Ativan, Xanax, restoril, CNS depressant used as hypnotic, anxiety can cause resp issues DONT stop abruptly taper off od right eye suspension prep shake before using CNS depressants benzodiazepines "lam & pam" Triazolam for management of insomnia do not use longer than 7-10 days at a time Avoid alcohol & smoking XL, DUR, SA dont chew or crush because it is meant to be long duration scheduled narcotics the lower the level # the stronger the narcotic Ex: #2 opiate #5 codeine Valsalva maneuver maneuver where pt is instructed to hold breath so catheter can be opened without letting air in H2 blockers ZANTAC TAGAMET DECREASE acid secretions os left eye liver patient diuretic Give potassium sparring diuretic (Aldosterone) NO salt subsitutes steroid usage temporment changes, eat constantly,decreases inflammation, watch for immune system compromise, sodium up, potassium down, glucose up, calcium down wt gain, BP up, muscle waiting, paper thin skin, SOLU-MEDROL IV taper off CNS depressants benzodiazepines "lam & pam" Flurazepam used to treat insomnia short term use GIve at BEDTIME check for signs of repiratory distress. AVOID ALCOHOL & other CNS depressants SE: hangover, light-headedness, dizziness, or confussion overdose: administer an EMETIC and follow w/activated charcoal/conscious pt or gastric lavage/unconscious pt administer ROMAZICON 1st inj NSAID Toradol narcotic agonist-antagonist Stadol mngmnt of mod-severe pain for cancer, renal calculi,labor,musculoskeletal, and burns. Obtain HX,monitor VS,bowel sounds, I/O SE: HYPOtension, constipation saline lock clean port, attach syringe, open slide clamp, aspirate back, flush, close slide clamp potassium (K+) K-Dur Micro-K Kaochlor excreted by Kidneys. TX HYPOkalemia which causes IRREGULA HEARTBEAT. LEVELS should be 3.5-5.3mEq/L assess for K+ depleting meds(lasix) EAT foods:OJ,raisins,bananas,potatos,dehydrated fruit. LABS: BUN,creatinine drink 6-8 oz of H2O. IV:DILUTE, NEVER BOLUS!!!WILL STOP HEART!can give IV piggy-back SE: n/v,diarrhea,abd cramps,rash antiparasitic FLAGYL

4 organisms of GI tract (H-pylori,giardia,trichomonis,C-Diff) used prior to GI surgery inhibits metabolism of anticoagulant in lice assess for CHRYSANTHEMUM allergy asssess for bleeding inhibits metabolism of anticoagulant in liver NO ALCOHOL SE: TACHYcardia,circulatory cllapse metallic taste,discolored urine expectorant Guaifenesin loosen bronchial secretions so they can be eliminated via coughing. Hydration is the BEST natural expectorant!take w. full glass of H2O BEFORE meals!if given w/meal increase risk of aspiration.SE: nausea,drowsiness, sedation Pepsin inhibitor Carafate adheres to ulcer to protect it.doesnt decrease acid. Take 1g QID BEFORE MEALS and BEDTIME glucose 70-110 nitrates off period 12hr if paste where gloves will get SE:HEADACHE too much ASA tinnitus give Vit K as antidote nephrotoxic (kidneys) hypertonic solution D5 pt with electrolyte loss from surgery sodium level 135-145 PICC line special RN to insert tunnel catheter long term Cytotec protects stomach lining from ulcers usually given w/NSAID course Aluminum can cause constipation proton pump inhibitor Prilosec, Prevacid , Protonix, Nexium BEST suppresses gastric acid secretion by inhibiting ATPase enzyme system in gastric parietal cells. inhibit gastric secretion 90% better than H2 antagonists. Take 1 hr PRIOR to FIRST MEAL of the day.dont crush or chew! Increases RISK of BLOOD BORNE ILLNESS. SE: HA,dizziness, diarhhea,abdominal pin Iron z-tract inj used to treat anemia know H&H if liquid drink through straw Vit K helps with absorption pc after meals central line need 10ml syringe or larger closed system flush w/NS med flush w/NS serum osmality level 280-296 Nitrates nitroglycerin dialates coronary arteries to up blood flow and oxygen and lowering workload and oxygen demand, and lower venous return.For chest pain. q5x3.may cause HYPOtension.AVOID alcohol

high bioavailability alot of medication is available for absorption too much tylenol antidote: mucamyst hepatoxic (liver) z-track inj (IM) iron get med out with one needle then change needle before injecting displace tissue to side, inject med wait 10 sec then remove needle and let go of skin flu/herpes (antiviral) Acyclovir treats HSV1/2, shingles po 5xd as left ear Mannitol diuretic used for intracranial pressure in ICU setting NPH insulin intermediate(2-4hrs) to cover next meal Fentanol used for procedural analgesic chronylac laxative LACTULOSE binds to ammonia and focally excreted.used w/liver failure, cirrhosis to decrease ammonia levels.very sweet inhaled acetylcysteine MUCAMYST antidote for tylenol toxicity. decreases thickness and stickiness of secretions. have suction available, assess respiratory status! beware of nausea and vomiting in pts. due to secretions. Assess lungs. Maintain Hydration! INR (heparin & coumadin) therapeutic range is 2-3 adregenic agonists adrenalin(epinephrine)nonselective (Beta 1-heart, Beta 2-lungs, alpha -vessels-vasoconstriction) stimulate the sympathetic nervous system treats allergic reaction,anaphylaxis,bronchospasm,cardiac arrest NO BETA BLOCKERS contradicted if client has cardiac dysrhymias, narrrow-angle glaucoma,or cardiogenic shock. ake w/food blood glucose may increase increases BP & HR dilates bronchial tubes SE: anorexia,n/v,nervousness,tremors,agitation,pallor,insomnia,syncope,TACHYcardia,dyspn ea,ventricular fibrillation,pulmonary edema lovenox 90 degree inj in "love handles" ARISTRA safest laxative psylium metamucil agonist starts something PPI and B12 need acid to absorb iron. B12 stored in liver for 5 years.Long term use of PPI...check B12 levels.May need supplement of B12 CNS depressants benzodiazepines "lam & pam" diazepam (valium) anxiety, stops seizures anti-platelet drugs Plavix

Used for prevention of MI or stroke. prevents aggregation in the ARTERIES. highly protein bound. PROLONGS bleeding time so STOP all anticoagulants and anti-platelets inluding ASA...7 days prior to surgery. DONT mix w/ garlic or gingko-risk of bleeding. OK to take Plavix with ASA. SE: GI bleeding, neutropenia.LABS: AST/ALT, bilirubin,creatinine, H/H.Evaluate liver function. narcotic agonist-antagonist Nubain relieve mod-sevre pain. Obtain drug HX. Use caution w/hx of drug abuse or emotional instability,impaired respirations, head injury,increased intracranial pressure,MI, biliary tract surgery, renal or hepatic dysfunction.. SE: dizziness, confussion,hallucinations,blurred vision,HA,flushing,sedation,nervousness,euphoria,bitter taste,dysphoria PT (coumadin) therapeutic range for someone on COUMADIN 2-3 fluoroquinolones AVELOX can cause tendon ruptures CNS depressants benzodiazepines "lam & pam" Ativan a preoperative sedative & to reduce anxiety,stops seizures Narcotic Codeine mild-moderate pain, cough suppressant. Use pain scale SE: drowsiness No alcohol adregenic agonist albuterol (proventil) selective-Beta 2 traets bronchospasm,asthma,bronchitis, & other COPD SE: tremor,dizziness,palpitations,reflex TACHYcardia,hallucinations,cardiac dysrhythmias CNS depressants benzodiazepines "lam & pam" alpraxolam (xanax) for alleviating anxiety that may cause sleeplessness antigungals "shake and bake" blood products at least 18 gauge needle, prime with NS 30 min to start transfusion from time you receive from blood bank can hang 4 hrs if reaction=stop transfusion and tear down everything and send to lab stimulant laxative DULCOLAX increases peristalsis by irritating sensory nerve ending. SE" N&V, abdominal cramping. Good for bowel prep CNS: Except for local anesthetics, all neuropharmacologic drugs act by altering synaptic transmissions. High selectivity. Three different effects of transmitter synthesis: Increase transmitter synthesis - storage vesicles will contain transmitter in abnormally high amounts. Decrease transmitter synthesis cause the transmitter content of vesicles to decline. Synthesis transmitter molecules that are more effective than the natural transmitter itself converts to a super transmitter. Peripheral Nervous System: two major divisions A) Autonomic Nervous System

B) Somatic Nervous System Employs three major transmittors ACh, Norepi, Epi Autonomic Nervous System: regulates many involuntary processes two major divisions A) Parasympathetic housekeeping B) Sympathetic fight or flight Parasympathetic Nervous System (functions): Slowing heart rate Increased gastric secretion Emptying of the bladder Emptying of the bowel Focusing the eye for near vision Constricting the pupil Contracting bronchial smooth muscle Sympathetic Nervous System (functions): Regulating the cardiovascular system Maintenance of blood flow to the brain Redistribution of blood flow during exercise Compensation for loss of blood, primarily by causing vasoconstriction Regulating body temperature By regulating blood flow to the skin Sympatietic nerves to sweat glands promote secretion of sweat, thereby helping the body cool By inducing erection of hair, sympathetic nerves can promote heat conservation Implementing the fight-or-flight reaction Increases heart rate and blood pressure Shunts blood away from skin and viscera and into skeletal muscles Dilates the bronchi to improve oxygenation Dilates the pupils (perhaps to enhance visual acuity) Mobilizing stored energy, therby providing glucose for the brain and fatty acids for muscles Parkinsons Disease: neurologic disorder characterized by tremor at rest, rigidity, postural instability and bradykinesia. Primary pathology is a degeneration of neurons in the substantia nigra that supply dopamine to the striatum. Result is an imbalance between dopamine and ACh. Disorder of the extrapyramidial system. Disrupts the balance between dopamine and Ach, dopamine is inhibited, ACh runs amuck [normally dopamine regulates ACh which controls movts] Anticholinergics used to primarily treat tremors; Levodopa is most common treatment of the disease. COMT inhibiters prevent breakdown of levodopa. Classes of drugs to treat Parkinsons: Anticholinergics block the cholinergic receptors Dopaminergics convert to dopamine

Dopamine Agonists stimulate the dopamine MAO-B Inhibitors - inhibit MAO-B enzyme which interferes with dopmaine COMT Inhibitors which inbits the COMT enzymw that maturates dopamine Levodopa/Carbidopa [Sinemet]: produces symptoms by promoting synthesis of dopamine in striatum. Follws via active transport into the brain across the BBB. Levodopa is needed because dopamine cannot cross into the brain alone decarboxylase convert levodopa into dopamine in the brain. Relieves symptoms by undergoing conversion to dopamine in surviving nerve terminals in the striatum. Carbidopa enhances the effects of levodopa by preventing the decarboxylation of levodopa in intestine and peripheral tissues. Since carbidopa cannot cross the BB, it does not prevent the conversion of levodopa to dopamine in the brain. Class: Dopamine agonist Indication: Goal of treatment is to improve the patients ability to carry out ADLs, does not cure but delays the progression. Pharmacodynamics/Kinetics: variable duration 6-12hrs. Administered orally and undergoes rapid absorption from small intestine. Only a fraction of each dose reaches the brain. Levodopa crosses by active transport. Adverse Effect: Nausea, vomiting, dyskinesias, cardiovascular (orthostatic hypotension, arrhythmia, chest pain, hypertension, syncope, palpation), psychosis, darkening sweat and urine.On-Off phenomenon. Drug Interactions: MAOIs (interaction causes hypertensive crisis), antipsychotics, anticholinergics, high protein meals (competes with protein) Combination with carbidopa allows levodopa dose to reduce by 75%, which can reduce some side effects Contraindications: hypersenstivity to levodopa, carbidopa or any component of the forumlation Precautions: pregnancy (c), diabetes, glaucoma, melanoma (or history of), renal/hepatic/cardiac disease, respiratory disease, MI, convulsions, peptic ulcer, lactation, depression.

Alzheimers Disease: A relentless illness characterized by progressive memory loss, impaired thinking, neuropsychiatric symptoms, and inability to preform routine tasks of daily living. Characterized by neuritic plaques, neurofibrillary tangles, and degeneration of cholinergic neurons in the hippocampus and cerebral cortex. Major risk factors: known risk factor is advancing age. Symptoms usually begin after after age 65. Family history is the only other known risk factor. Treatment: Donepezil [Aricept] cholinesterase inhibitors; increases the availability of ACh at the cholinergic synapses and thereby enhance transmission by cholinergic neurons that have not yet been destroyed by Alzheimers. Produces modest improvement in cognition, behavior and function in 30-60% of patients. Does not cure, but slow progression for a time. Choice drug for mild to moderate AD. Well absorbed by oral administration, metabolized by hepatic enzymes, elimination is mainly urine and partly in the bile. Prolonged plasma half-life (about 60hrs), administered once a day. Adverse

Effects: GI upset, nausea, dizziness, headache, diarrhea, bronchoconstriction, use with caution in COPD and asthma patients. Interactions: drugs that block cholinergic receptors can reduce the effects. Memantine [Namenda] 1st representative of new class of drugs. Works on the NMDA receptor antagonists. Approved for moderate to severe AD, only modest beneficial effects. Appears devoid of significant adverse effects; constipation, dizziness, confusion, headaches. PO, well absorbed. Largely excreted unchanged in urine. Long half-life (6080hrs). Plasma levels peak (3-7hrs). Interactions: undesirable effect when combination with other NDMA antagonists. Seizures: Intiated by discharge from a group of hyperexcitable neurons, called a focus. Partial seizures: excitation undergoes limited spread from the focus to adjacent cortical areas Generalized seizures: excitation spreads widely throughout both hemispheres of the brain Antiepileptic drugs: act through four basic mechanisms blockade of sodium channels blockade of calcium channels blockade of receptors for glutemate potentiation of GABA Traditional AEDs - well established, extensive experience, less expensive, less tolerated, less safe Newer AEDs - introduced in late 1993 or later, equally good but less established, safer,limited interactions, less extensive, more expensive Goal of Epilepsy: goal is reduction seizures to an extent that enables the patient to live a normal or near-normal life. Complete elimination of seizures may not be possible without cauing intolerable side effects. Selective per seizure: Many AEDs are selective for particular seizures, and hence, successful treatment depends on choosing the correct drug. Withdrawal: must be done very gradually because most cause CNS depression and abrupt withdrawal can trigger Status Epilepticus. Phenytoin [Dilatin]: active against partial seizures and tonic-clonic. Not active against absence seizures. Capacity of liver to metabolize is limited, so doses only slightly greater than those needed for therapeutic effects can push phenytoin levels into toxic range [small therapeutic range] Therapeutic range: 10-20mcg/ml Levels > 20mcg/ml results in CNS toxicity. S/S include: nystagmus, sedation, ataxia, diplopia, and cognitive impairment. Adverse effects: also includes gingivial hyperplasia in 20% of patients Class: Antiarrhythmic agent, anticonvulsant (suppresses Na+ influx) Indication: active against partial seizures, as well as primary tonic-clonic Mechanism: Causes selective inhibition of sodium channels, but slowing the recovery of Na+ channels from inactive state to active state. Pharmacokinetics: Absorption varies, liver has a limited capacity to metabolize. Small

changes in dose can disproportionately affect serum levels small increases cause toxicity, small decreases cause therapeutic failuer. Half-life varies. Adverse Effects: CNS effects (nystagmus, diplopia, ataxia), Gingival hyperplasia, skin rash, hypotension, dysrrhythmias. Valporic Acid [Depakote]: Very broad spectrum antiepileptic. Active against parital seizures and most generalized seizures, including tonic-clonic, absence, atonic and myoclonic. Can cause potentially fatal liver injury. Can also cause potentially fatal pancreatitis. Therapeutic level: 50-100mcg/ml Cardiovascular Thereapies : CAD, CHF, HTN, Cholesterol, Anticoagulation Remodeling: theprocess in which the ventricles dilate and hypertrophy, thus increasing wall stress and reducing left ventricular ejection fraction. Preload: the work imposed on the heart before the contraction begins. The amount of blood pumped with each beat. Afterload: the pressure that the heart muscle must generate to move blood into the aorta. The work presented to the heart after contraction has finished. Starlings Law: SV = CO x HR Ejection Fraction: direct indicator of left ventricular function [the amount of blood pumped at of the left ventricle into systemic system]. 65% or greater EV is normal. ACE-Inhibitors: Affects the angiotensin-aldosterone system. Used in the treatment of HTN, HF, and diabetic neuropathy. Reduces levels of angiotensin II [a potent vasoconstrictor] this causes vasodilation, reduces blood volume, reduces cardiac and vascular remodeling, causes potassium rentention and fetal injury; it also increases levels of bradykinin[vasodilation] which results in vasodilation, cough and angioedema (rare). Only med that improves ventricular function (works on cardiac afterload reduction, which increases cardiac output). Adverse effects: hypotension, persistent cough, hyperkalemia, renal failure, Fetal injury, angioedema. Contraindicated: pregnancy (2nd or 3rd trimester) [ex: Captopril, Lisinopril]ARBs: Similar to ACE except there is no cough. Work by blocking angiotension, but do not work on bradykinin so there is no cough or hyperkalemia. These decrease the release of aldosterone and increase renal excretion of Na+ and water. [ex: Losartan, Valsartan] Calcium-Channel Blockers: Prevent calcium from entering cells. When calcium channels are blocked, contraction will be prevented and vasodilation will result. In the heart it causes myocardium (decreases myocardial contractility), SA Node (reduces heart rate) and AV Node (decreases velocity of conduction through the AV node). In stable angina, CCB work to decrease oxygen deman by dilating arterioles, which decrease afterload, and by decreasing heart rate and contractility. Adverse effects: constipation, peripheral edema, hypotension, AV-block. Used as first line therapy in African-Americans because Beta-Blockers are ineffective. Nitrates: Indicated for HTN, Angina, HF, and MI.in stable angina they decrease oxygen demand

by dilating veings, which decreases preload. In variant angina they increase oxygen supply by relaxing coronary vasospasm. Lipid soluble, administration PO/ SL. Metabolized in the liver. Adverse effects: postural hypotension, relflex tachycardia [ex: nitroglycerin] In event of CP: take one tablet, wait 5 min, another tablet, if no relief call 911, take a 3rd tablet in five minute while waiting for paramedics Statins: (HMG-CoA reductase inhibitors)Reduction of LDL cholesterol, possible elevation of HDL cholesterol. Nonlipid beneficial cardiovascular actions reduce the risk of CV events, increased bone formation. Mechanism of reducing cholesterol is complex and dependent non the increasing of LDL receptors on hepatocytes. Adverse effects: headache, rash, GI upset, myopathy/rhabdomyolysis(rare), hepatotoxicity (rare). Interactions: Fibrates and ezetimibe, Agents that inhibt CYP3A4. Contraindicated: Pregnacy [ex: Atrovastatin (lipitor), Simvastatin (zocor)] FYI: when a person comes into the ED with an MI, they are immediately placed on Zocar to lower LDL Diuretics: Drugs that can increase the output of urine. Used for the treatment of HTN, mobilization of edematous fluid, prevention of renal failure. They work by blocking Na+ and Cl- reabsorption. By blocking the reabsorption of solutes, diurectics create osmotic pressure within the nephron that prevents the passive reabsorption of water. The increase in urine flow is directly related to the amount of Na+ and Cl- reabsorption it blocks. Drugs whose site of action is early in the nephron block the great amount of solute reabsorption and produces the greatest amount of diuresis. Adverse effects: hypovolemia, acid-base imbalance, disturbance of electrolyte levels. LOOP DIURECTCS: most effective diurectics available. Produce more loss of fluid and electrolytes. Site of action: Loop of Henle. [ex: Furosemide (Lasix)] THIAZIDE DIURECTICS: Similar effects to loop diuretics. Increases renal excretion of Na+, Cl-, K+ and water. Elevate plasma levels of uric acid and glucose. Diuresis is considerably lower than loop diuretics. [ex: Hydrocholorthiazide (HCTZ) ] POTASSIUM-SPARING DIURETICS: produce a modest increase in urine produce a substantial decrease in K+ excretion. Blocks the actions of aldosterone in the distal nephron: causing retention of K+ and increased excretion of Na+. [ex: Spironalactone (Aldectone)]. Beta Blockers: Beta blockers work to balance oxygen demand by slowing the heart rate and contractility, which allows for a more effect contraction, reducing cardiac output. They also can suppress reflex tachycardia. Long term use reduces peripheral vascular resistance. The major consequences of beta blockers include: 1) reduced heart rate 2) reduced force of contraction and 3) reduced velocity of impulse of conduction through AV-node. They are used int the treatment of HTN, but also HF, hyperthyroid, migraines and stage fright. Biggest side effect is fatigue, these patients are very hypotensive. Adverse effects: Bradycardia, AV-hear tblock, HF, bronchoconstriction, CNS effects. They can mask the signs of hypoglycemia so routine blood sugar levels should be taken. [ex: metoprolol (lopressor), propranolol (inderol)]

Vasodilators: Indicated for HTN, angina, HF and MI. Adverse effects: postural hypotension, reflex tachycardia. [ex: Hydralazine (Apesoline)] Furosemide [Lasix]: Inhibits reabsorption of sodium and chloride channels at proximal and distal tubule and in the loop of henle. Class: Loop diuretic Indication: Treatment/management of pulmonary edema, edema in CHF. Hepatic disease, nephrotic syndrome, ascites, HTN Pharmacokinetics: Onset: diuresis PO 30-60mins IM 30mins IV 5mins Peak: PO 1-2hrrs. Duration: PO 6-8hrs IV 2hrs. Absorption: PO 60% -67%. Protein binding >68%. Metabolism: minimally hepatic. Half-life in normal renal function: 0.51.1hrs, ESRD 9hrs. Excretion: Urine within 24hrs (PO 50%), feces as unchanged drug. Crosses the placenta and is excreted into breast milk. Adverse Effects: Headache, fatigue, acute hypotension, Ototoxicity, electrolyte disturbances, acid-base imbalances, renal failure, hypergylcemia. Precautions: Pregnancy (c), diabetes, dehydration, severe renal disease, cirrhosis, ascites. Contraindications: Hypersensitivity to sulfonamides, anuria, hypovolemia, infants, lactation, electrolyte depletion. Digoxin [Digitek]: Indicated for HF and control of dysrhythmias. When used for HF, it can reduce symptoms, increase exercise tolerance and decrease hospitalizations. However in women, may shorten life. Exerts a positive inotropic aciton on the heart which increases the force of ventricular contraction and increase CO. Kickstarts the heart. Typically given with a loading dose of 1.25mg in 4 doses within 24hours. Hold digoxin if HR<50. You would expect to give a PT presenting with CHF in the ED a loading dose. Therapeutic levels: 0.8 - 2 Class: Antiarrhythmic agent, Cardiac glycoside Indication: Treatment of CHF, and to slow ventricular rate in tachyarrhythmias such as Afib, Aflutter, and supraventric tachyc; cardiogenic shock. Pharmacokinetics: PO onset: 30m-2hrs, peak 6-8hrs, duration 3-4days IV onset: 5-30mins, peak 1-5hrs, duration variable. Absorption is by passive nonsaturable diffusion in the upper small intestine. Distribution in normal renal function is 6-7L/kg, in chronic renal failure its only 4-6L/kg. Extensive peripheral tissue distriubtion. Hyperkalemia/hyponatremia causes a decreased digoxin distribution to heart and muscles. Metabolism is via sequential sugar hydrolysis in stomach or by reduction of lactone ring in intestinal bacteria. Metabolism is reduced in CHF. Bioavailability is 7080% tablet. Half-life depends on age, renal and cardiac function. Half-life elimination is about 1.5 days, excreted via urine. Adverse Effects: Headace, fatigue, drowsniess, 1st or 2nd degree heart block (wenckebach). Dysrrhythymias, hypotension, nausea, vomiting. Dig-toxicity: extreme vomiting. Precautions: Pregnancy (c), renal disease, acute MI, AV-block, severe respiratory disease, hypothyroidism, geriatric sinus nodal disease, lactation, hypokalemia. Contraindications: Hypersensitivity to digoxin, Vfib, ventricular tachycardia,

carotid sinus syndrome, 2nd or 3rd degree heart block. Interactions: Beta-Blockers increase bradycardia, Diuretics/corticosteroids/certain antibiotics cause hypokalemia and dig toxicity. Thiazides and IV calcium cause hypercalcemia, dig toxicity. Warfarin [Coumadin]: Goal is to prevent thrombosis without inducing spontaneous bleeding. Gold standard treatment for Afib. Baseline assessment: Medical history, VS, INR, CBC, History of alcohol abuse. Give orally and monitor INR closely. Adverse effects: Bleeding and hemorrhage. Long-term treatment decisions: typically standard of care, keep on coumadin for 6 months, then discuss pros & cons, if goes off and has a recurrence then back on for life. Antagonist of vitamin K. Blocks four clotting factors that are dependent on vitamin K. Overdose can be overcome with vitamin K. Binds 99% with albumin. This binding provides basis of several drug interactions INR is a blood test that measures coumadin levels. Therapeutic ranges: 1.6 2.0 joint replacement/abdominal surgery 2.03.0 Afib, CVA, recurrent DVT, PE (longterm management) 2.5 3.5 Mechanical Valve Repair Class: Anticoagulant Indication: prophylaxis and treatment of thromboembolic disorders and embolic complications arising from atrial fibrillation. Adjunct to reduce risk of systemic embolism after myocardial infarction. Mechanism: Supresses coagulation by acting as an antagonist of vitamin K. By antagonizing vitamin K, warfarin blocks the biosynthesis of vitamin K-dependent clotting factors (VII, IX, X and prothrombin), which reduces fibrin production. Pharmacokinetics: Binds 99% to albumin in the blood. Unbound molecules can readily cross membranes (including placenta and milk-glands). Undergoes hepatic metabolism and is excreted in urine and feces. Onset: 24-72hrs, peak (full therapeutic effect) 5-7days, duration 2-5 days, absorption: rapid and complete, distribution: 0.14L/kg, half-life elimination 20-60hrs [1.5-2days]. Adverse Effects: Bleeding and hemorrhaging Precautions: Breast-feeding Contraindications: pregnancy (X), hemorrhagic tendencies, spinal cord/eye/brain surgeries. Interactions: drugs that increase the effects of warfarin [ex: aspirin, sulfonamides, acetaminophen], drugs that promote bleeding [ex: aspirin, heparin, glucocorticoids] and drugs that decrease effects of warfarin [ex: phenytoin, rifampin, vitamin K, OCPs, carbamazepine, phenobarbital] Heparin: rapid acting anticoagulant. Unable to cross membranes (including GI tract), must be given subQ or IV. Goal is to prevent thrombosis without spontaneous bleeding. Must guac stools everytime PT moves bowels. Assess BP, HR, CBC, platelet counts, PTT. Before you start heparin you want to you normal clotting abilities. Heparin specifically enchances the activity of antithrombin, which is a protein that inactivates thrombin and factor Xa [production of fibrin becomes reduced and clotting is suppressed].

Preferred anticoagulant for use during pregnancy aPTT = activated partial thromboplastin time (IV heparin monitoring) normal value is 40secs for someone not heparin No monitoring for subQ Therapeutic Ranges: 60-80secs Levels <60: dosage needs to increase Levels >80: dosage needs to decrease Class: Anticoagulant Indication: prophylaxis and treatment of thromboembolic disorders Mechanism: Inactivates antithrombin which supresses thrombin and factor Xa leading to a reduction in the production of fibrin. Pharmcokinetics: unable to cross membranes, cannot be absorbed orally. Must be given IV or subQ. Does not enter placenta or breast milke. Binds nonspecifically to plasma proteins. Plasma levels of free heparin can be IV or subQ. Hepatic metabolism, renal excretion. Half-life is short (1.5hrs). Adverse effects: hemorrhage and thrombocytopenia Precautions: People who have a high likelihood of bleeding, severe disease of the liver and kidney. Contraindicated: thrombocytopenia and uncontrolled bleeding. Also in people post-surgery of eye, brain or spinal cord. Interactions: Any drugs that depress platelet function (ex: aspirin) will weaken this defense and must be employed with caution Low-weight Molecular Heparin [Lovaenox and Fragmin]: unfractionated heparin. Advantages are that they are given on a fixed schedule, may be used at home, are dosed once a day, based on body weight. No monitoring necessary, SubQ administration, more expensive. Spironolactone [Aldactone]: Blocks the actions of aldosterone in the distal nephron. By inhibiting aldosterone there is a retention of potassium and an excretion. Diuresis is minimal. Class: potassium-sparing diuretic Indication: Primarily hypertension and edema, CHF, hypokalemia, ascites or liver disease accompanied by edema or ascites. Pharmacokinetics: Onset 24-48hr, peak 48-72hr, metabolized by liver, excreted in urine, crosses placenta. Protein binding 91% - 98%. Hepatic metabolism. Half-life elimination 78-84hr. Excretion urine and feces. Adverse Effects: Hyperkalemia, which can cause fatal dysrhythmias. Discontinue if K+ rises above 5 or if signs of hyperkalemia develop. (injection of insulin can help reduce K+ levels) Precautions: dehydration, liver disease, renal impairment, electrolyte imbalances, metabolic acidosis, lactation Contraindications: pregnancy (D), hyperkalemia, renal disease, anuria, Hypersensitivy. Interactions: Thiazide and loop diuretics counteract potassium-wasting effects. ACE-inhibitors and other drugs that raise K+ levels. Never combine with K+ supplements or salt substitutes.

IV. Diabetes and Thyroid Thyroid hormone: stimulates energy use (metabolism), stimulates heart, promotes growth and development. Feedback Loop: TRH - TSH - TH [amount of TH shuts on or off TRH/TSH] Increased TSH : hypothyroidism. (the anterior pituitary releases increased TSH to stimulate thyroid gland to decrease TH in blood) Decreased TSH: hyperthyroidism. (too much T3 and T4 in circulation which is an inhibitor of release of TSH) Hypothyroidism: slows body down. Gain weight, fatigue, lethargy, puffy face, britle hair, heart rate lowered. Levothyroxine: Thyroid hormone replacement therapy. Converted T3 in the body. Highly protein-bound. Prolonged half-life (7 days). Requires one month to reach plasma levels. Structure is identical to natural TH. Monitor serum TSH levels. Normal TSH levels 0.3 6. Less than 0.3 is hyper; greater than 6 is hypo class: thyroid hormone-replacement indication: hypothyroidism, myedema coma, some thyroid cancers action: increases metabolic rate, controls protein syntehsis, increase CO, renal blood flow, and oxygen consumption. Increases body temp, blood volume, growth development. Exact mechanisms are unknown. pharmacokinetics: oral onset 3-5days, IV onset 6-8hrs, duration 1-3wks, peak 6-8wk. Oral absorption is erractic, take in morning 30mins before meals to enhance absorption. Protein binding >99%, hepatic metabolism. Half-life 3-4 days. Doesnt readily cross placenta, minimal amounts in breast milk. Excreted in feces via bile. Adverse Effects: Thyroid storm, anxiety, insomia, tremors, headache, tachycardia, cardiac arrest, palpitations, diarrhea, heat intolerance, weight loss [similar to hyperthyroidism] Precautions: pregnancy, geriatric, angina, lactation, renal insufficiency, diabetes, CAD, hypertension, ischemia. Contraindications: Adrenal insufficiency, recent MI, alcohol intolerance, thyrotoxicosis Interactions: Iron supplements [give 2 hrs after dosage], maalox, calcium-supplements (tums), questran Reduce drug absorption Coumadin, catecholimines (dopamine, epi), zoloft, tegretal, dilantin Accelerate effects of drug. Thyroid storm: critical, life-threatening, hyperthermia, tachycardia, restlessness, afitation and tremor. Extreme exacerbation of thyrotoxicosis. Diabetes I: beta-cell destruction usually leads to absolute deficiency. Polyuria, polydipsia, polyphagia, weight loss. Usually juvenile, abrupt onset. Insulin is sole treatment for survival. Diabetes II: insulin-resistance and ineffective insulin secretion which reduces binding of insulin to receptors, reduces receptor number and reduces receptor responsiveness. Eventually hyperglycemia leads to destruction of pancreatic beta-cells and insulin production and secretion decline. Usually over 40, gradual onset, family

history, asymptomatic, frequently obses, excerise and lifestyle changes are essential Short-term complications: hyper-, hypo-glycemia, ketoacidosis Long-term complications: Micro [renal, retino, nephro] and macro [cardio]vascular complications. Insulin is required and only treatment for gestational diabetes (pregnancy). HgA1C < 7 3 month-look back blood glucose control Proper diet: carbs + monosaturated fats 60-70% of energy intake Protein 15-20% of energy intake Polysaturated fats 10% of daily energy intake Saturated fats <10% of energy intake Cholesterol limited to 300 mcg/day -Rapid-acting [lispro/humalog]: Onset = 15 30mins Peak = 30mins 2.5hrs Duration = 3 6.5 hrs Eat within 15 mins of administration. Feed insulin. -Short-Acting [regular/Humalin R]: Onset : 30mins 60mins Peak : 1 5hrs Duration : 6 -10hrs Only type of insulin that can be given IV -Intermediate-Acting [NPH/Humalin N]: Onset : 60 120mins Peak : 6 14hrs Duration: 16 24hrs Clear to cloudy when mixing, roll the vial -Long-Acting [Lantus/Glargine]: Onset: 70mins Peak: none Duration: 24hrs Never mix Lantus with anything For all insulins monitor for signs and symptoms of hypoglycemia -Metformin [Glucafage]: oral agent for type II diabetes. Balances out the body by increasing insulin uptake in the muscles and decrease glucose production by liver. Does not cause hypoglycemia. Number one side effect diarrhea. Class: biguamide, antidiabetic Indication: type II diabetes Pharmacokinetics: Onset within days, max up to 2wks. Distrubtion by RBCs, absorbed slowly in Small Intestine. Not metabolized by liver. Bioavailibilty absolute. Plasma half-life 6.2hrs, blood half-life 17.6hrs. Excreted by the kidneys (urine). Extended release take with biggest meal, regardless of what time of day. Adverse Effects: Diarrhea, GI upset, headache, lactic acidosis, nausea, Vomiting. Precautions: Pregnancy (use insulin), hypersensitivity, geriatric, thyroid disorder. Contradindications: Creatinine over 1.5 (males), 1.4 (females), renal disease, CHF, alcoholism, history of lactic acidosis, cardiopulmonary disorder. No

contrast for CT scan, hold for 48 hrs prior, check renal function post-scan. Interactions: increase metformin levels Tagamet, digoxin, alcohol, morphine, vanco. Increase hypoglycemia Tagamet, calcium channel blockers, corticosteroids, estrogens, diuretics, dilantin COPD/Asthma Short acting vs long acting inhaler usage Albuterol [short acting]: Beta-2 agonist used for patients with asthma and COPD. Usually PRN for athsma attacks. Adverse effects: tachycardia, angina and tremor. Bronchodilates in a reversible airway obstruction opens airway:, prevention of exerciseinduced bronchospasm. Always watch vitals. Most patients administer incorrectly. Use only for ongoing, acute attacks (or prevention of exercise-induced). 2 puffs every 4-6hrs. Wait one minute between each puff. If administering a short and long-acting inhaled med, take the short-acting first to open airways then administer the long-acting (aka albuterol first then steroid). Salmeterol [long acting]: Beta-2 agonist long term control. Dosed on fixed schedule. Not used for acute episodes. When incorrectly may increase risk of athsma related death. Not first agents for long-term control, should be used alone. Use in combination steroid treatments (advair). One inhalation every 12 hours. Inhaled Glucocorticoids: Suppresses inflammation. Decreases synthesis and release of inflammatory mediators. Decreases infiltration and activity of inflammatory cells. Decreases edema of the airway mucosa. Combination of Fluticasone with Salmerterol is Advair. Typically in powder form. Adverse effects: Oralpharyngeal candidiasis (thrush) and dysphonia (hoarseness). Patient needs to gargle after administration. Check blood sugar with diabetes because steroids can increase blood glucose levels. VI. RA/OA/Osteoporosis General meds used for treatment of Osteoarthritis (pain in tendons and joints): -NSAIDs [asprin] (COX-I inhibitors) great risk of GI bleed, alleviate mild to moderate pain and inflammation -Celecoxib [celebrex] (COX-II inhibitor) reduced risk of GI bleed because does not decrease platelet aggregation, works on pain and inflammation -Acetaminophen lacks anti-inflammatory properties, works to reduce pain General meds for treament of RA: -DMARDS [disease modifying anti-rheumatic drugs) Acetominophen [tylenol]: Anti-pyretic, non-opioid analgesic. Indicated in mild pain and fever. Does not suppress platelet aggregation, does not suppress renal blood flow, does not cause renal impairment, does not cause gastric ulceration. Mechanism of action: inhibits synthesis of prostaglandins that may serve as mediators of pain and fever primarily in the CNS. Well absorbed orally, crosses placenta and breast milk (in low concentrations),

widely distributed, metabolized in liver, metabolites may be toxic in overdose concentrations, half-life 2hrs, excreted in urine. Overdose can cause severe liver damage. No more than 4g/day, always count. Use with caution in hepatic disease, renal disease, alcoholism, malnutrition. Interacts with alcohol because consumption increases risk of liver injury. Interacts with Coumadin, puts at risk for bleeding. Interacts propanolol, decreases metabolism and may increase effects. Concurrent NSAIDS increase risk of renal effects. Monitor LFTs. Alendronate[Fosamax]: Bisphosphonate, treatment of osteoporosis. Inhibits bone reabsorptions by increasing activity of osteoclasts. Food decreases absorption. Adverse effects: difficulty swallowing [esophogitis], esophageal ulcers, dysphagia, constipation. Contraindicated in renal insufficiency, pregnancy, lactation. Patient education includes, take first thing in the AM 30 mins before food or other meds. Take with a full glass of water and do not lay back down for 30 mins (keep patient upright) to prevent reflux could leave hole in esophagus. Interactions include calcium supplements, antacids and oral meds that may decrease absorption. Dose 10mg/day. NSAID Therapies [Asprin, Ibuprofen, Celebrex]: Non-steroid anti-inflammatory. Used for treatment of osteoarthritis, rheumatoid arthritis, and gout. (Cox-1 mediates housekeeping chores: gastric protection, kidney function, platelets. Mediates beneficial processes. Cox-2 primarilty at the site of tissue injury, mediates inflammation and sensitizes receptors to pain. Mediates harmful processes.) NSAIDs are COX-inhibitors. Huge risk for GI bleed, except Celebrex has a lower risk because does not suppress platelet aggregation. Cox-2 inhibitors can impair renal function and cause HTN and edema, increase the risk of MI and stroke. Aspring can cause tinnitus (ringing in ears) with levels above 200mcg/ml. LAB VALUES K+ 3.5 5.0 Cr 0.5 - 1.2 BUN 10 30 Na+ 135 145 BNP 0 - 100 [know for HF]