NR 508 Week 4 Anti-depressants and Anti-anxiety/Anti-insomnia agents and read Depression, pharmacology for psychosis, bipolar disorder, anxiety, and ADHD

· NR 508 Week 4: Lesson – listen to lectures on Anti-depressants and Anti-anxiety/Anti-insomnia agents and read Depression, pharmacology for psychosis, bipolar disorder, anxiety, and ADHD. Some of the questions on the midterm may come from these lectures. (Questions are at the end of the ppts) · Reading assignments: Refer to week 4 Reading in the modules · Week 4: Midterm Exam the midterm is 50 questions, each worth 2 points for a total of 100 points. Requires the use of Respondus Lockdown Browser, due to be completed by Sunday 11:59PM Mountain time. Please note week 4 lesson and reading assignments will be covered in the midterm. 1. Know first-line treatment for Heart Failure (CHF). ACEI (-pril)- through halting the production of angiotensin II, ACE inhibitors result is arterial dilation and a systemic lowering of blood pressure. Cardiac muscle cells are more easily nourished with blood, reducing workload caused by narrowed vessels. CCB (pine)- result in myocardial muscle cell and vessel relaxation. This is because CCBs prohibit the influx of calcium, a muscular stimulant, into the heart muscle. Heart rate, blood pressure, and myocardial oxygen demand are all reduced. In addition, angina pectoris and arrhythmias can be alleviating through the myocardial relaxation caused by CCBs. ARB (sartan)- which are generally used if the patient is unresponsive or intolerant of ACE Inhibitors, block the already present angiotensin II, not allowing the hormone to result in vessel narrowing. ARBs aid myocardial blood flow, particularly in the coronary arteries, by allowing arterial relaxation. Contraindicated in angioedema or C1 interase patients Diuretics- Diuretics, including thiazides, help in alleviating hypertension by allowing salt and water to be excreted through the urine at a faster rate. Diuretics decrease systemic volume and thus systemic pressure, reducing the workload of the heart. THIAZIDE & CCB for AA 2. Know the treatment of Acute heart failure and pulmonary edema. Diuretics- 1. thiazide- HCTZ- distal tubule 2. loop- Lasix & bumex- most potent- acute heart failure with edema- loop of Henle 3. potassium-sparing- spironolactone- collecting duct (least potent) 4. Know the side effects of ACE inhibitors and mechanism of action of ACE inhibitors. ACEIs block angiotensin-converting enzyme (ACE), which is responsible for the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor and is a stimulus for aldosterone release from the adrenal glands (Figure 22-1). Reduction in aldosterone secretion results in less water absorption and sodium/potassium exchange in the distal renal tubule, causing a slight increase in serum potassium. ACEIs inhibit the breakdown of bradykinin, a potent and naturally occurring vasodilator, by blocking the enzyme kininase II. This is thought to be the cause of the cough commonly experienced by patients who take this class of drugs. Side effects- dry cough, hyperkalemia, fatigue, dizziness, headaches, loss of taste 5. Know which antihypertensive medication classes are contraindicated in patients with asthma. Beta blockers & ace inhibitors? Beta blocker are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors. Therefore, beta-blockers are sympatholytic drug 6. Know the mechanism of action of Digoxin. 7. Digoxin has an inotropic effect on cardiac cells caused by enhancement of excitation-contraction coupling triggered by membrane depolarization. It acts at the cellular membrane by inhibiting the sodium-potassium pump, thus causing an increase in intracellular sodium. This increases sodium/calcium exchange and subsequent calcium accumulation in the sarcoplasmic reticulum. Activation of cardiac contractile proteins, actin, and myosin follows. The overall result is increased force of contraction of the cardiac muscle. 8. Cardiac glycosides (1) increase the force of myocardial contraction; (2) depress the sinoatrial node by stimulating vagal activity; (3) prolong conduction to the AV node via vagal stimulation; (4) increase the refractory period of the AV node; and (5) increase peripheral resistance. HR is slowed both vagally and extravagally. Monitor for Toxicity • • To monitor for toxicity, the health care provider must be alert to early signs of toxicity and must obtain a serum level. A digoxin level 2 ng/ml indicates toxicity, although some patients become toxic at lower doses. Serum levels should be drawn at least 6 to 8 hours after the last dose and, ideally, just before the next dose. • • Hypokalemia is a risk factor for the development of arrhythmia even in patients within the therapeutic range. The earliest signs of digoxin toxicity are subtle and are easy to ignore: increased fatigue, visual disturbances, sinus bradycardia, anorexia, weakness, and nausea. 6. Know the uses and mechanism of action of Penicillin. Mechanism of Action Penicillin is a derivative of 6-aminopenicillanic acid that is composed of a distinct four-membered β-lactam ring fused to a five-membered thiazolidine ring; this constitutes the chemical structure. Penicillin subclasses have additional chemical constituents that bestow differences in antimicrobial activity, susceptibility to acid, enzyme hydrolysis, and biodisposition. Many biosynthetic types of penicillin have been created through the introduction of diverse acids, amines, or amides into developing penicillin molds, to render products superior to the natural penicillins. Penicillins, which are bactericidal against susceptible organisms, disrupt synthesis of the bacterial cell wall and compete for and bind to specific enzyme proteins that catalyze transpeptidation and cross-linking. The enzymes to which they bind are called penicillin-binding proteins (PBPs). They consist of transpeptidases, transglycosylases, and D-alanine carboxykinase and are implicated in the final phases of building and reshaping of the bacterial cell wall while it is growing and dividing. This action interferes with the biosynthesis of mucopeptides and prevents linkage of structural components of the cell wall. After the penicillin molecules bind and inhibit the transpeptidase enzymes, susceptible bacteria are no longer able to lay protein cross-links across the peptidoglycan backbone of the cell wall. In addition to being structurally weak, this formation is thought to catalyze the activation of autolytic enzymes in the cell wall that cause progressive bacterial lysis. Treatment Principles • • Oral penicillins generally are indicated for the treatment of mild to moderately severe infection caused by penicillin-sensitive microorganisms. These broad-spectrum antibiotics are used as empirical treatment for many infections, according to the site of infection, in some cases while the results of a culture are awaited. • • All penicillins, with the exception of amoxicillin, are absorbed better when taken on an empty stomach. • • Many penicillins, including penicillin G (IM), penicillin V, cloxacillin, dicloxacillin, amoxicillin, and amoxicillin and potassium clavulanate (AM/CL), are indicated as first-choice empirical treatment for many infections, including skin infections, animal bites, otitis media, sinusitis, pharyngitis, acute exacerbation of COPD, syphilis, mastitis, and Lyme disease (see Table 59-1). Penicillin V remains the drug of choice for group A β-hemolytic streptococcus. Penicillin G remains the drug of choice for syphilis. • • A minimum of 10 days of treatment is recommended for any infection caused by group A β-hemolytic streptococci, to prevent the occurrence of acute rheumatic fever or acute glomerulonephritis. In severe staphylococcal infection, continue therapy with penicillinase-resistant penicillins for at least 14 days. • • The natural penicillins are generally active against non–penicillinase-producing staphylococci and streptococci and most gram-positive organisms. They also are active against some gram-negative cocci such as Neisseria and against most anaerobic bacteria. Natural penicillins, if the bacteria are not resistant, are more effective against gram-positive bacteria than are semisynthetic penicillins. Penicillin V (oral) can be used instead of penicillin V (IM, IV), except against gram-negative species such as penicillinase-producing Neisseria gonorrhoeae and Haemophilus. • • The aminopenicillins are active against all of the bacteria that penicillin G is active against, along with non–penicillinase-producing staphylococci, some streptococci, and some gram-negative cocci and enterococci. The addition of a β-lactamase inhibitor product to the treatment regimen expands the spectrum to include greater numbers of gram-positive and gram-negative bacteria and anaerobes. The combination of amoxicillin and clavulanate is commonly used intravenously and increases the spectrum of amoxicillin effectiveness to cover S. aureus, Moraxella catarrhalis, Haemophilus influenzae, Salmonella, and Shigella. • • Penicillinase-resistant penicillins are used for the treatment of infections caused by penicillinase-producing staphylococci and some streptococci that have demonstrated susceptibility to the drug. They may be used to initiate therapy in suspected cases of resistant staphylococcal infection prior to the availability of susceptibility test results. Do not use in infections caused by organisms susceptible to penicillin G. • • The carboxypenicillins are less active than the ureido-penicillins against streptococci and Haemophilus spp. • • The ureidopenicillins have increased the activity of penicillin against gram-negative and anaerobic bacteria, including Pseudomonas. Together, the third- and fourth-generation agents are known as the antipseudomonal penicillins. • • Extended-spectrum penicillins are effective in treating Pseudomonas aeruginosa; this is commonly seen in patients with cystic fibrosis. How to Monitor • • Monitoring is particularly important in newborns and infants, and when high dosages are used. • • Perform bacteriologic studies to identify causative organisms and to determine their susceptibility, so that appropriate therapy is administered. • • Monitor for resolution of the infection and for resistance, especially to community-acquired MRSA. • • Clostridium difficile infection of the bowel may develop. • • Penicillin G potassium can cause hyperkalemia. • • Penicillin G with procaine: Monitor for sensitivity to procaine. • • Penicillinase-resistant penicillins: Obtain blood cultures, WBC, and differential cell counts prior to initiation and at least weekly during therapy with penicillinase-resistant penicillins. Measure liver transaminase AST and ALT levels during therapy to monitor for liver function abnormalities. Perform periodic urinalysis, BUN, and creatinine determinations during therapy, and consider dosage alterations if these values become elevated. If renal impairment is known or suspected, reduce the total dosage and monitor blood levels to avoid possible neurotoxic reactions. • • When administering penicillin parenterally, the practitioner should monitor the patient for at least 30 minutes post-administration to rule out any allergic or anaphylactic reaction to the drug. • • Avoid subcutaneous and fat layer injections; pain and induration may occur. • • Inadvertent intravascular administration of IM injections has resulted in severe neurovascular damage. Damage has occurred after injections into the buttock, thigh, and deltoid areas. These reactions occur most frequently in infants and small children. • • Some products contain tartrazine and sulfites. 7. Know they uses, mechanism of action and side effects of Beta Blockers. Uses of beta blockers- angina, decrease bp, abnormal heart rhythms, anxiety, migraine, glaucoma MOA- block the effects of a hormone called epinephrine/adrenaline. Heart beats slower; decreases BP Side effects of BB- dizzy, weak, fatigue, drowsy, dry mouth/eyes, headache, upset stomach, diarrhea/constipation 9. Know the uses mechanism of action and side effects of Tetracyclines. 10. Lyme disease 11. •Acute exacerbation of COPD 12. •Sinusitis 13. •Pneumonia 14. •Chlamydia 15. •Rickettsial infections 16. •UTIs MOA- The tetracyclines are bacteriostatic antibiotics. Their mechanism of action is to inhibit protein synthesis in the susceptible organism by binding to the 30S ribosome subunit, thereby impeding the binding of aminoacyl tRNA to the receptor site on the messenger RNA ribosome complex. Tetracyclines also may reversibly bind to 50S ribosomal subunits and may alter cytoplasmic membranes of susceptible organisms, resulting in leakage of cytosolic nucleotides. This action requires active microbial growth that distinguishes tetracyclines as bacteriostatic rather than bactericidal agents. Side effects- nephrotoxicity, esophagitis, swollen tongue/difficulty swallowing, mild nausea/v/d, swelling of genitals, vaginal itch/discharge, photosensitivity 9. Know the usage of Antiarrhythmics and the mechanism of action and side effects of Antiarrhythmic Agents. Paroxysmal svt/a fib/ premature ventricular contractions Used for fast, slow, or irregular heart beats Mechanism of Action Antiarrhythmic drugs act to reduce electrical irregularity of the heart. They do this by altering the action potential of cardiac cells (Figure 23-4, Table 23-2). All antiarrhythmics have the potential to cause arrhythmia. In 1995, CAST (Cardiac Arrhythmia Suppression Trial) revealed the dangers of aggressive medical treatment of arrhythmias. Class IA drugs (quinidine, disopyramide, procainamide) depress rapid depolarization (phase 0) of the action potential. These drugs act to slow conduction by lengthening the effective refractory period of atrial and ventricular myocardium, by depressing the inward sodium current, and by decreasing the automaticity and excitability of ectopic foci of cardiac muscle. Class IB drugs (lidocaine, mexiletine, tocainide) exert less effect on sodium channels at rest but are more prominent during depolarization, so their effect on phase 0 is only slight. Class IC drugs (flecainide, propafenone) depress phase 0 markedly and profoundly slow conduction. β-Blockers are Class II antiarrhythmics that work by inhibiting sympathetic stimulation. They antagonize the effects of catecholamines released from the adrenergic nerve endings and the adrenal medulla. Blocking sympathetic activity reduces the rate of discharge of the sinus and other foci that act as pacemakers, and it increases the effective refractory period of the AV node. Class III drugs (amiodarone, dronedarone, ibutilide, dofetilide, sotalol) prolong phase 3 repolarization by blocking potassium channels. The QT interval is thus prolonged on the ECG. This prolongation also increases the risk of torsades de pointes, a ventricular tachycardia. Amiodarone, however, does not appear to have this effect. Amiodarone blocks sodium channels, and this contributes to slowing of conduction and prolongs refractoriness in the AV node. Its vasodilatory action decreases cardiac workload and therefore decreases myocardial oxygen consumption. Dronedarone is a benzofuran derivative of amiodarone that was recently FDA approved. A high mortality rate in patients with atrial fibrillation taking this drug makes it questionable whether it will remain on the market. There is some indication it prolongs the QT interval. Sotalol exhibits β-blocking activity. Ibutilide is available only as an IV formulation and is used for rapid termination of atrial fibrillation and flutter. Dofetilide must be initiated in a hospitalized patient because of its ability to prolong the QT interval. 10. Know the treatment of Parkinson’s disease Levodopa/Sinemet- a natural chemical that passes into your brain and is converted to dopamine Dopamine agonists (not as effective as levodopa, but may work in conjunction) doesn’t convert into dopamine, but mimics the effects of dopamine on the brain 11. Know the first line treatment of depression. SSRI- Lexapro, celexa, paxil, Zoloft SNRI- Effexor, Cymbalta NDRI- Wellbutrin 12. Know the preferred antidepressants used in the elderly (less anticholinericc effects) - the SSRI Paroxetine should be avoided due to an increase in drug interactions and also more anticholinergic effect than other SSRIs; Older adults are more prone to hyponatremia with SSRIs than other populations. 13. Know the adverse effects associated with SSRIs Drowsiness, nausea, dry nouth insomnia, diarrhea, nervousness, sexual problems, headache, blurred vision 14. Know medications used to treat Depression medications including SSRIs SNRIs; 15. Know which SSRIs can be used in children Prozac over the age of 8 17. Know how to treat Alzheimer’s Disease Cholinesterase inhibitors- Aricept, Exelon, razadyne & memantine- namenda 18. Know the first-line treatment for generalized seizure management 19. Know the side effects of Carbamazepine and what lab monitoring is required Tegretol- nausea, vomiting, dizzy, drowsy, dry mouth, swollen tongue, unsteady, loss of balance- Monitor- 20. Know which common drugs require serum level monitoring 20. Know the role of the NP in practice and what guides NP practice. 21. Know mechanism of action for oral contraceptives pills; contraindications of oral contraceptives. 22. Know the mechanism of action of Antiprotozoal agents 23. Know antifungal medications and which antifungals treat different diseases and fungal infections 24. Know contraindications when prescribing contraceptive management 25. Know treatment for Generalized Anxiety disorder 26. Know treatment for ADHD, side effects, and monitoring 27. Know the role of the Drug Enforcement Administration 28. Know the treatment for GERD