Pharm_ week 1-.docx

Pharm: Week 1- Kahoot username: Kkatsade Pharmacology: the study of medications Drug: a substance capable of producing a biological response Medication: a drug given to produce a therapeutic response *a drug and a medication cannot always be classified the same* Pharmacology: Effective use of drugs...

Pharm: Week 1- Kahoot username: Kkatsade Pharmacology: the study of medications Drug: a substance capable of producing a biological response Medication: a drug given to produce a therapeutic response *a drug and a medication cannot always be classified the same* Pharmacology: Effective use of drugs and medications by a health care team depends on being able to apply knowledge related to: Anatomy and physiology Pathophysiology Chemistry Microbiology Nursing process Therapeutics: The branch of medicine concerned with the prevention of disease and treatment of suffering Classification of drugs: Traditional medications: Produced by pharmaceutical manufacturer Biologics: agents produced by animal cells and microorganisms Hormones, antibodies, vaccines Natural health products Natural plant extract Vitamins, minerals Dietary supplements Prescription drugs: Requiring a dispensing order (prescription) from a qualified health care professional before patient receiving the drug benefits: Healthcare providers can examine patients before ordering medication, ensuring the order is appropriate for the patient and condition The dose and frequency of dispensed drugs can be controlled The patient was provided with education about the drug including dosing, interactions, adverse effects Over-the-counter drugs (OTC): Drugs that patients can obtain without consultation with a health care provider: benefits: Usually, they have a higher margin of safety and few adverse effects Patients can treat themselves for common conditions by following directions of packaging Convenience Disadvantages: Not always safe even if OTC May not be taken properly Not properly educated Prescription vs OTC: Depending on the dose and formulation, a particular drug may be available PTC or may require a prescription Prescription drugs require more patient education than OTC drugs OTC drugs, if not taken for appropriate reasons may be ineffective, allowing the patient's condition to become worse Contraindications: someone who could be hypersensitive to the drug and cannot take it Drug regulations and standards: Drug regulations were created to protect the public from drug misuse and to assume continuous evaluation of safety and effectiveness Test on health subjects without disease to see if no adverse effects were present Biologics and genetic therapies directorate: Parallel branch to TPD that regulates biologics and radiopharmaceuticals Natural and non-prescription health products directorate Parallel branch to TPD that regulates natural health products A seven step process that includes preclinical and clinical trials, pre market review and approval and post-market evaluation Step 1: preclinical trials using cultured cells, living tissues and small animal models Step 2: clinical trial application and testing Phase l -> health subjects (evaluate safety of drug and possible adverse effects) Phase ll -> small group of patients with target condition Phase lll -> large group of patients with target condition Step 3: manufacturer completes new drug submission (NDS) to health canada Outlines test data obtained from clinical trials, indication. Adverse effects, production and packaging Step 4: committee of drug experts reviews NDS to identify benefits and risks Step 5: health canada shares information about drug with health care providers and consumers Step 6: if approved, health canada issues a drug information number (DIN) and a notice of compliance to manufacturer Both required for marketing drug Health canada continues to evaluate drug safety and efficacy through quality assurance processes Term Definition Indication Conditions for which the drug is used Contraindication Prototype drug Generic vs trade Therapeutic index Measure that compares LD50 (toxic dose) and ED50 (effective dose) using a ratio TI = LD50/ED50 Half-life The duration of action, how long does it take for the concentration of the medication to drop First-pass effect When the drug is absorbed and starts to become metabolized by the liver it can become inactivated Potency vs efficacy Potency: the dose of medication required to produce a particular response Efficacy: the magnitude of maximum response to a drug Pharmacodynamics Area of pharmacology concerned with how drugs produce change in clients and differences in client responses to medication Pharmacokinetics To the movement of a drug through the body Loading dose Repeated dosing to get to the therapeutic range more rapidly Controlled substances Drugs that affect the central nervous system that have high potential for abuse and addiction Combination drugs Mechanism of action Kidneys eliminate the most drugs, and can also be eliminated through: Sweating Breastfeeding Feces Urine Drug-drug interactions: medications that cannot interact with each other Drug-food interactions: grapefruit juice can increase the interaction of certain medications (BP medication), some medications cannot have dairy, etc Characteristics of an ideal drug: Effectively prevents, treats or cures condition of patient Easy to administer Produces rapid, predictable response at relatively lose doses Rapid onset of action Duration of action appropriate to reaching therapeutic goals Rapid elimination of drug No adverse effects No interactions with food or other drugs No contraindications - safe for all patients to take Inexpensive and accessible Classification of drugs: Therapeutic classification Describes the condition for which a medication is being given (ex, antihypertensive) Pharmacologic classification Describes the mechanism by which the therapeutic effect is achieved (ex, beta blockers, diuretics, ACE inhibitors) Medications can have multiple classifications Indication Condition or circumstances for which the drug has been approved A particular drug may have multiple indications Mechanism of action Means by which drug carries out a therapeutic effect Ex, a diuretic (pharmacologic class) reduces blood pressure (therapeutic class) by reducing blood volume (mechanism) Both therapeutic and pharmacologic classifications are useful but limited Therapeutic class identifies purpose of drug (indication) but now how it works (mechanism of action) Pharmacologic class identifies mechanism but not indication Multiple pharmacologic classes can be used for a single therapeutic class Multiple therapeutic classes can be addressed with a single pharmacologic class Within a pharmacologic class, there are often many different but related versions of a drug Prototype drug - a representative drug from a class that is used as a point of comparison for related versions of that drug Learning one drug can allow nurse to extend knowledge to other similar drugs within that class Generic name: name adopted by regulatory agencies to describe active ingredient of a drug Ex, diazepam Trade name: proprietary name used by the company that produces a drug Ex, valium Drug schedules in canada: Schedule l Available only by prescription and provided by a pharmacist, includes the following: All prescription drugs Drugs with less potential for abuse (schedule F) Controlled drugs (schedule G) Narcotic drugs Schedule ll Available only from a pharmacist, must be retained in an area with no public access Schedule iii Available via open access in a pharmacy or pharmacy area (over the counter) Unscheduled Can be sold in any store without professional supervision Controlled drugs and substances act: Categories controlled drugs and substances into 8 schedules Opioids Cannabis Psychotropics LSD, ecstasy, psilocybin, methylphenidate CNS depressants Barbiturates, benzodiazepines Anabolics Precursors Outlines penalties based on offense related to controlled drug Possession Production Possession for exportation Trafficking Includes narcotic control regulations Pharmacokinetics: Refers to the movement of a drug through the body Describes what the body does to a drug as it enters the blood, as it moves to target tissues, as it is metabolized and as it is removed from the body Drugs must pass a series of barriers to reach target tissue Depends on physiologic processes Drug must reach target tissue at high enough concentration to produce at a therapeutic effect Nurse must be aware of how many factors may impact of drug that reaches target tissue Route of administration Patient characteristics Four processes of pharmacokinetics Absorption How drug reaches the circulation Movement of drug from site of administration to circulation Primary factor for determining onset of drug action Quantified as bioavailability Factors affecting rate of absorption Route of administration Enteral, parenteral, topical Increase dose = increases rate of absorption due to increased concentration gradient Factors affecting rate of absorption GI tract environment Presence of food may decrease absorption Presence of certain foods and drugs may alter rate of absorption Motility - influences time during which absorption can occur Blood flow and surface area increased blood flow = increase rate of absorption Increase surface area = increase rate Route of administration Impact of temperature on blood flow Factors affecting rate of absorption Drug ionization Depending on pH of surrounding fluid, most drugs in either charged or uncharged state Acids are absorbed in acids because they are nonionized Bases are absorbed in bases because they are unionized Acid in a basic environment is ionized and therefore less able to cross membrane Distribution How drug reaches target tissue Transportation of drugs throughout body to target tissue Factors affecting distribution of drug Blood flow to target tissue Increased blood flow = more drug reaching target tissue Drug solubility Hydrophilic drugs transported in solution Lipophilic drugs - a portion is bound to plasma proteins (ex, albumin); a portion of drug is in solution Drug must move from circulation to target tissues to create response Special barriers to drug distribution Blood brain barrier Does not contain pores Protects brain from pathogens and toxins Only lipid-soluble drugs to cross Not fully developed in neonates Inflammation can increase permeability Special barriers to drug distribution Fetal-placental barrier (FPB) Prevents harmful substances from passing mothers blood stream to fetus Permeability of barrier changes during pregnancy However, some drugs can cross (alcohol, cocaine, caffeine, some prescription meds) Pregnancy categories for drugs Must consider if patient is of childbearing age prior to prescribing a drug Metabolism How drug is altered by body Process by which structure (and function) of drug, nutrients, vitamins, and minerals is altered Liver is primary site for metabolism Metabolism usually makes drug more excretable Structural changes result in functional changes to drug Microsomal enzymes in liver carry out most metabolic activities Cytochrome P450 (CYP) An enzyme that metabolizes many drugs Many isoenzyme systems within CYP Determine speed at which drug is metabolized Ability of patient to metabolize drugs changes throughout life cycle Infants lack mature microsomal enzyme systems Enzyme activity often reduced in older adults Ability of patient to metabolize drugs influenced by many factors Decreased metabolism with liver impairment Genetic variations of CYP enzymes Excretion How drug is removed from body Removal of drug from the body Kidney is primary site for excretion Pulmonary, glandular, fecal excretion Rate of excretion influences concentration of drug in blood Renal excretion Most drugs are filtered into the nephron but not reabsorbed (drug remains in urine) pH of urine can influence reabsorption of drug from nephron Renal excretion Damage to kidney usually reduces excretion of drug thus dose reduction may be necessary for renal patient Pulmonary excretion Glandular secretion Drugs can be secreted in saliva, sweat, breast milk Consideration for nursing mother Fecal and biliary excretion Drugs taken via enteral route may not be fully absorbed and are excreted in feces Enterohepatic recirculation Time-response relationships: Goal of nurse is to maintain drug at a concentration (therapeutic range) in blood that produces a therapeutic response Plasma drug levels rise as drug is absorbed and then decrease as drug is excreted If plasma levels exceed the therapeutic range (toxic range), drug is more likely to produce more adverse effects Therapeutic range can be very narrow Onset: time from point at which drug is administered until it reaches a therapeutic range Duration: time period in which drug concentration is in a therapeutic range Termination: time period from when drug is administered until its concentration drops out of a therapeutic range Drug half life: provides estimate of duration of action, time for concentration of drug to be reduced to 50% Maintaining plasma concentration within therapeutic range requires careful dosing Must consider magnitude and frequency of doe, as well as drug half-life More than 90% of drug is excreted after four half-lives Repeated dosing required to maintain steady plasma concentration of drug Next dose given before plasma concentration dips out of therapeutic range Sometimes it is important for a drug to reach a therapeutic range more quickly Loading dose is given Larger dose that leads to more rapid absorption and shorter onset of action Maintenance doses are given to maintain drug within therapeutic range Pharmacodynamics: Refers to what the drug does to the body to create a response Related to the mechanism of action of a drug Related to how a drug interacts with a target tissue Nursing process Recognizing that there is a considerable variation in client response to a particular dose of a drug Recognizing consequences of giving too much or too little of a drug in terms of therapeutic response, risk of adverse effects Application of pharmacodynamics critical for safe and responsible administration of medications Interpatient variability: Response to dose of a drug is normally distributed across a population Some people require a very small dose to produce a therapeutic response Some people require a very large doe to produce a therapeutic response Most require a dose in the middle to produce a therapeutic response Interpatient variability - ED50 Dose at which 50% of a population exhibit desired therapeutic response Clinical implications Predicts dose range to achieve therapeutic response ED50 may be toxic for some patients and may not produce a meaningful response in others Critical to monitor patient response to assess if dosage adjustments is indicated TD50 and LD50: Normal frequency distributions exist for both the dose of a drug at which it is toxic and at which it is lethal for test subjects TD50 refers to median toxic dose Dose at which 50% of test subjects exhibit a response indicative of toxicity LD50 refers to medial lethal dose Dose at which 50% of test subjects are killed by drug Therapeutic index (TI): Measure that compares LD50 and ED50 using a ratio TI = LD50/ED50 If a drug has a large TI, it is considered to be a safer then a drug with a smaller TI Graded dose-response relationship: Describes relationship between dose of drug and intensity of drug response Sinusoidal curve with three distinct phases Phase 1: occurs at low doses, very little change in response as dose increases Phase 2: linear phase, sharp increase in response as dose is increased Phase 3: plateau phase, no change in response as dose increases Phase 2 is the best range of doses to achieve a safe, therapeutic effect Response to drug usually due to several mechanisms More receptors being affected by drug More enzymes being affected by response Patient symptoms affected by drug Ex, patient has a headache and feels better after taking medication Phase 1: Few receptors or enzymes affected, therefore response is minimal Phase 2: As more receptors or enzymes are affected, intensity of response increases Phase 3: Plateau phase Drug is bound to all receptors or enzymes, or symptoms have been alleviated. Increasing the dose has no further effect Potency and efficacy: Not all drugs produce the same intensity of response Two measures are commonly used to quantify and compare elements of graded dose-response curves Potency Efficacy Potency: Amount of drug required to produce a particular intensity of response Drug that required lowest dose to produce a particular intensity of response is most potent Efficacy: Max intensity of response produced by a particular dose of drug Drug with greatest intensity of response has highest efficacy Agonists and antagonists: Some drugs are better at stimulating intracellular responses than others Agonist Mimics the action of endogenous substances, the response may be greater than endogenous activity Partial agonist Produces weaker responses than endogenous substances Antagonists Prevent action of endogenous substances, usually by competing with endogenous liquid and/or agonist for receptor binding sites Sometimes used to prevent adverse effects of overdoses Antagonists do not usually have intrinsic activity Pharmacogenetics: Branch of pharmacology that studies the role of genetic variation in drug responses Considers underlying genetic expression as reason for why drug therapy not effective for everyone Human growth and development: Growth: progressive increase in body size as individual ages into adulthood Development: functional evolution of physical body and of psychomotor and cognitive abilities Normal growth and development includes the following phases: pregnancy/ prenatal Infancy Toddlerhood Preschool School age Adolescence Young, middle and older adulthood Consider impact on pharmacokinetics related to medication Physical development considerations Route of administration (is there factors that could impact route and formulation of medication) Maturity of liver and kidney (is patient able to adequately metabolize drug? Is the patient able to excrete medications?) Psychomotor development considerations Route of administration (is there factors that could impact route and formulation of medication) Cognitive development considerations Patient education (is the patient able to appreciate the need for a medication or the risks associated with it?) Pregnancy: Pharmacotherapy during pregnancy must be undertaken with great caution Caring for two individuals Where possible, alternative therapies should be considered before initiating pharmacotherapy Some conditions require the use of medication Pre-existing or developed conditions not related to pregnancy Conditions that affect the well-being of the fetus The developmental stage of embryo/fetus Particular caution should be taken during the first three months Teratogens – substances that promote abnormal growth in the fetus; dose and timing are key considerations All drugs assigned to a “pregnancy category”, developed by US Food & Drug Administration (see table 6.1), and adopted by Health Canada Pregnancy categories: 6 categories (A, B,C, D,X, N) used as guides for healthcare providers Testing of drugs is typically performed in animal models Extrapolation of results to humans is limited due to differences in the fetal placental barrier between species Some testing has been done with human subjects Category Definition A Adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal abnormalities. Example drugs: levothyroxine and folic acid B Animal studies have revealed no evidence of harm to the fetus; however, there are no adequate, well-controlled studies in pregnant women. or Animal studies have shown an adverse effect, but adequate, well-controlled studies in pregnant women have failed to demonstrate a risk to the fetus. Example drugs: metformin and pantoprazole C Animal studies have shown an adverse effect and there are no adequate, well-controlled studies in pregnant women. or No animal studies have been conducted and there are no adequate, well-controlled studies in pregnant women. Example drugs: gabapentin and prednisone D Studies, adequate, well-controlled, or observational, in pregnant women, have demonstrated a risk to the fetus; however, the benefits of therapy may outweigh the potential risk. Example drugs: lisinopril and lorazepam X Studies, adequate, well-controlled, or observational, in animals or pregnant women have demonstrated positive evidence of fetal abnormalities. The use of the product is contraindicated in women who are or may become pregnant. Example drugs: atorvastatin and warfarin N The FDA has not yet classified the drug. Example drugs: aspirin and acetaminophen Category A and B: Considered safe for use during pregnancy Category C The most common assigned category Should be avoided if possible Higher doses associated with teratogenic effects Category D and Category X Should not be taken during pregnancy Category N No studies have been done in animal models or during pregnancy in humans Pharmacotherapy during pregnancy: Physiologic changes during pregnancy can alter normal pharmacokinetic responses Most body systems undergo predictable changes during pregnancy that health care must understand when prescribing drugs to the pregnant woman Pharmacotherapy during lactation: Breastfeeding Provides nutrition, emotional bonding, and immune protection to neonate The majority of drugs secreted into breast milk to some extent The majority of mothers breast-feed their newborns Most medications will reach breast milk Factors that impact the amount of drug that enters breast milk Plasma concentration in maternal blood Higher concentration in maternal blood means more drugs in breast-milk Drug characteristics Lipid solubility – lipophilic drugs pass more easily Size – small molecules pass more easily Half-life – short t1/2, less likely to pass Plasma protein binding – drug molecules bound to plasma protein do not cross, though drug in solution can cross Response of infant to medications in breast milk: The drug enters GI tract of the infant Stomach content is quite acidic which can damage and denature some drugs Drug absorbed through the small intestine is subject to first-pass metabolism though the infant liver is not yet mature Kidneys are also immature so clearance of drugs may be slower Some drugs are contraindicated during breastfeeding Adverse effects in infants during lactation Nonspecific drug effects Diarrhea Constipation Sedation Irritability Drug-specific effects Related to the action of the drug Pharmacotherapy throughout the lifespan - prenatal: Pre-implantation period (weeks 1 – 2) Little vascular connection thus drugs in maternal circulation have little effect Embryonic period (weeks 3 – 8) Most rapid development of internal structures thus teratogens can have the most impact during this period Fetal period (weeks 9 – 40) Organ systems continue to develop The fetal placental barrier becomes more permeable thus greater sharing between maternal and fetal circulations Maternal liver and kidney disease can have a profound effect on drug levels in the fetus Important to differentiate between effects associated with pregnancy and adverse effects of medications Pharmacotherapy throughout the lifespan - infancy: Extends from birth to one year of age The focus is on the safety and comfort of the infant during pharmacotherapy Education of parents is key for the administration of drugs, assessing for adverse effects Administration of drugs by a nurse Note differences in muscle mass Sites for IV insertion Pharmacotherapy throughout the lifespan - toddlerhood: Extends from 1 – 3 years of age Parent teaching is key as toddlers can resist taking medications Short concise explanations before administering Dosing is usually by body weight Adverse effects tend to manifest is the same way as they do in adults Keep medications out of reach of toddlers Pharmacotherapy throughout the lifespan - school age: Extends from 3 – 12 years of age Similar considerations as for toddlers when giving medication up to about age 5 or 6 Short direct explanations and praise for successful administration work better From ages 6 – 12, rapid growth and development during this period Direct explanations that include the rationale for taking medication are effective as this group tends to be more cooperative Give limited choices to create a sense of control Common problems are GI and respiratory Pharmacotherapy throughout the lifespan - adolescence: Extends from 13 – 18 years of age Rapid growth and psychological development Important to fit in and to be treated as an individual Risk of recreational drug use Parents should be aware of the common effects of marijuana, etc Parents should be aware of performance-enhancing drugs Common needs for pharmacotherapy Skin problems Headaches Menstrual symptoms Sex-related concerns Eating disorders Alcohol and tobacco use Sports-related injuries Many adolescents will not admit to a lack of knowledge regarding drugs or condition Pharmacotherapy throughout the lifespan - young adulthood: Extends from age 18 – 40 Generally the healthiest period of adulthood Requiring few prescriptions aside from contraceptives; compliance is good Risks for the 18 – 24 age group include substance abuse Pharmacotherapy throughout the lifespan - middle adulthood: extends from 40 – 65 years of age Stress is more common leading to a variety of chronic health issues Work Sandwich generation Common chronic health conditions include Cardiovascular disease Obesity Arthritis Cancer Pharmacotherapy throughout the lifespan - older adulthood: Age 65 and beyond Improved longevity and quality of life have led to a greater risk of chronic health disorders Adverse effects more common in period Compliance Changes to body as part of aging; degeneration of organ systems Multiple illnesses and medications Polypharmacy – multiple prescriptions to address multiple health concerns increased risk of adverse effects and interactions Compliance can be challenging – multiple pills at different times during the day Pharmacokinetic changes Absorption Slower compared to middle adulthood Increased gastric pH Decreased gastric motility Decreased blood flow to the GI tract Distribution Decreased fluid volume Increased concentration of hydrophilic drugs Decreased lean muscle mass/increase in body fat Lipophilic drugs may be stored in adipose, diminishing the plasma concentration of the drug Decreased production of albumin May increase the concentration of free lipophilic druG Decreased cardiac output Distribution Decreased cardiac output Reduce the rate of distribution to target tissues The brain barrier becomes more permeable May increase the concentration of some drugs in the CNS Metabolism Decreased production of enzymes by the liver Metabolism is slowed Reduced first-pass metabolism Excretion Blood flow decreases Fewer functional nephrons Renal function declines The glomerular filtration rate decreases. Decreased rate of excretion for many drugs Can extend the half-life of a drug Considerations for successful pharmacotherapy in older adults Drug adherence Complicated by declining sensory abilities Complicated by declining cognitive function Polypharmacy – complicated regimens Financial/accessibility Promoting adherence in the older adult client Reasons for nonadherence Unpleasant adverse effects Forgetfulness Cognitive or physical impairment Poor or misunderstood instructions Complicated regimens Inability or refusal to purchase the medication Health beliefs about medications Ways the nurse can promote adherence Assist the older adult in comprehending and committing to the drug treatment regimen. Communicate the instructions in such a manner that the older patient fully understands the purpose of the treatment. Provide the older patient with social support services to obtain the medications. Work with a pharmacist to ensure that the medication is dispensed in containers that are easily opened and in formulations that are easily taken. Make sure all drugs are clearly labeled with instructions. Simplify the regimen to reduce the number of drugs and doses per day. Suggest that the older patient use a daily or weekly pill counter. Provide the patient with a check-off calendar to document each time a medication is taken. Engage family members or friends in supporting the older patient in their efforts to comply. Encourage the older patient to report signs of adverse effects. Schedule periodic tests to determine plasma drug levels. Place follow-up calls to high-risk patients. Week 2: The process of hemostasis: Three major steps Intrinsic and extrinsic pathways both lead to the formation of prothrombinase Prothrombinase converts prothrombin to thrombin Thrombin converts fibrinogen to fibrin Fibrin strands trap RBCs to form a clot Role of platelets Platelets adhere to and aggregate at the site of injury in the vessel Platelet activation leads to the formation of fibrin network that traps RBCs forming clot Role of cofactors in hemostasis Ca+2 and vitamin K are critical for the synthesis of clotting factors in clotting factors Fibrinolysis Plasmin breaks down fibrin network Pharmacotherapy focuses on manipulating these elements Process of Fibrinolysis: Plasmin breaks down fibrin network Thromboembolic disorders: Thrombus -> stationary clot Embolus -> a clot that moves to another location Deep venous thrombosis (DVT) Venous clots often develop in the legs as a DVT, but can migrate to lungs creating a pulmonary embolism Clots migrating from left atrium can cause strokes Coronary artery clots cause MIs Mechanism of Coagulation modifiers: Anticoagulants: Heparin: *med card* Enhances antithrombin lll (AT-lll) activity Decreases thrombin activity (active factor lla) Decreases prothrombinase activity (active factor Xa) Low molecular weight heparin: Also enhances AT-lll activity but more specific to prothrombinase (active factor X) Fewer adverse effects than heparin Less risk of thrombocytopenia compared to heparin Gets broken down in the GI tract, will given subcut and IV, not orally Heparin Therapeutic effects and uses Acute thromboembolic disorders including DVT, pulmonary embolism, unstable angina, evolving MI Prophylaxis for clotting Mechanism of action Activates antithrombin lll, which inhibits thrombin and factor Xa (Prothrombinase) Prevents clot formation, does not break down existing clots Adverse effects Mild allergic symptoms Osteoporosis Skin lesions Serious adverse effects Abnormal bleeding Heparin-induced thrombocytopenia Causes by abnormal antibodies that activate platelets, causing clots to form and depleting platelet counts in blood Is moitored by activated partial thromboplasti times (aPTTs) Is available in parenteral form Has a short half-life (1.5 hours) Has as it antidote protamine sulfate (codamine sulfate) Nursing implications Intravenous (IV) doses are usually double-checked with another nurse Ensure that subcutaneous doses are given subcutaneously, not intramuscularly Subcutaneous doses should be given in areas of deep subcutaneous fat, and sites should be rotated Do not give subcutaneous doses within 5cm of: The umbilicus, abdominal incisions, open woulds, scars, drainage tubes, stomas Do not aspirate subcutaneous injections or massage injection site May cause hematoma formation Low molecular weight heparins: Less side effects Less laboratory monitoring Given subcutaneously Warfarin (Coumadin) Therapeutic effects and uses Prophylaxis of thromboembolic events DVT Pulmonary embolism Prophylaxis arterial thromboembolism Prevention of CVA/MI Prevent clotting in long-term indwelling catheters Mechanism of action Inhibits the action of vitamin K Adverse effects Mircoembolism Osteoporosis, bone fractures Serious adverse effects Abnormal bleeding Antidote Vitamin K Prothrombin time (PT): Used to monitor effectiveness of warfarin Normal range is 12-15 seconds Therapeutic warfarin therapy requires PT to increase 1.5-2 times the clients baseline International normalized ratio (INR): A standard measurement of PT INR values averaging 2.5 considered therapeutic for most indications A normal range for INR is about 1 (without being on anticogaulations) Transitioning from IV heparin to PO warfarin: 2 drugs administered simultaneaously for 2 to 3 days (related to half-life of each) Nursing considerations for patients receiving anticoagulant therapy: Assessment Obtain a complete health history including allergies and drug history Obatin baseline vital signs, especially heart rate and blood pressure, and clotting times Planning Patient to experience decrease in blood coagulability based on changes to clotting times obatind during assessment Provide education regarding drug action, precautions, and possible adverse effects Interventions Monitor for signs of excessive bleeding Monitor vital signs with emphasis on blood pressure and heart rate Monitor for signs of excessive clotting Monitor CBC Monitor patients with kidney or liver disease, GI, diabetes with extra care Platelet activation and aggregation: At sites of damage to endothelial cells, platelets adhere to vessel wall, then become activated Activation leads to aggregation of platelets into clumps, promoting the formation of clots Signaling and connection between platelets depends on receptors Antiplatelet drugs: Antagonizing these receptors prevents platelet aggregation, thereby preventing clot formation Antiplatelet drug example Asprin Reduces formation of thromboxanes (promote activation of platelets) Acetylsalicylic acid (ASA): Low dose used for anti platelet MOA: inhibits platelet aggregation Use as anticoagulant: reduction of risk of mortality following MI, reduces stroke incidence Adverse effects: GI discomfort and bleeding contraindicated with other anticoagulants due to increased bleeding potential Acetylsalicylic acid (ASA) MOA inhibits platelet aggregation Use as anticoagulant reduction of risk of mortality following MI, reduces stroke incidence Adverse effects GI discomfort and bleeding contraindicated with other anticoagulants due to increased bleeding potential Role of nurse Monitor for bleeding Risk increases if given with anticoagulants Prolonged pressure needed to control bleeding at puncture sites Monitor for gastrointestinal upset with aspirin May increase menstrual bleeding Common pulmonary disorders: Asthma COPD (chronic bronchitis, emphysema) Common cold Respiratory system: Responsible for exchange of oxygen (O2) and carbon dioxide (CO2) between blood and atmosphere (respiration) Air passes through the nose, pharynx, larynx, trachea, bronchi, bronchioles, and alveoli (ventilation) Gas exchanges occurs between alveoli and pulmonary capillaries Physiology of the lower respiratory tract: Bronchi have smooth muscle that allows them to change diameter, controlled by autonomic nervous system Sympathetic nervous system Causes bronhciolar muscle to relax and bronchodilation to occur Parasympatheic nervous system Causes bronchiolar muscle to contract and bronchoconstriction to occur Airways narrow due to bronchospasm Narrowed brochi impairs ventilation Pathophysiology of asthma: Chronic inflammation, resulting in: Increase in airway edema Increased mucous secretions Smooth muscle constriction in bronchioles Signs and symptoms Difficulty ventilating lungs Tachypnea Gasping for air Pharmacotherapy of asthma: Drugs are given to either terminate an episode or to prevent episodes Most drugs are given topically via inhalation route in the form of aerosols Drug is delivered to site of action rather than to whole body Systemic side effects are less likely via inhalation though they can still occur Difficult to measure the exact dose that reaches alveoli; proper education on use of delivery system is essential for success Administration of pulmonary drugs via inhalation: Most adverse effects are local (mouth and throat) but some drug is swallowed and absorbed causing systemic effects Delivery routes Metered-dose inhaler (MDI) Emits of puff of drug that is inhaled by patient Dry powder inhaler (DPI) Delivers drug as a fine powder, using a propellant, during inhalation Nebulizer Liquid drug is vapourized into mist and inhaled Pharmacotherapy of asthma drugs that can terminate episodes: Beta2-adrenergic agonists Promote bronchodilation Most frequently prescribed drugs for treatment of bronchoconstriction Available in PO, inhaled and parenteral formulations Classified by duration action Short-acting – quick onset, 2 – 6 hr duration Intermediate-acting – slow onset, 8 hr duration Long-acting – slow onset, 12 hr duration, not suitable for acute episode Salmeterol (Servent, diskhaler disk) Therapeutic uses and effects Long-acting beta2 agonist indicated for prevention of asthma epiosdes in patients with severe persistent asthma Chronic bronchitis Mechanism of action Stimulates beta2 receptors in smooth muscles of bronchioles promoting bronchodilation and improved airflow and ventilation Adverse effects Throat irritation Headache Restlessness, insomnia, nervousness Dry mouth Serious adverse effects Tachycardia, chest pain Paradoxical bronchospasm Allergic response Tremor Pharmacotherapy of asthma drugs that can terminate episodes: Methylxanthines: Long-term management of asthma when beta agonists, anticholinergics do not work Chemically similar to caffeine Nausea, vomiting, CNS stimulation are common adverse effects Inhaled anticholinergics: Promote bronchodilation by blocking muscarinic Ach receptors Alternative to short-acting beta2 agonists Can be combined with beta2 agonists Decongestant Phenylephrine (Neo-synephrine): Selective alpha-adrenergic agonist used for common cold to relieve nasal congestion Intranasally by spray or ddrops to reduce nasal congestion by constricting small blood vessels in the nasal mucosa Can cause buring of nasal mucosa and rebound congestion if used for prolonged periods Only use for up to 3-5 days Nursing considerations for patients receiving bronchodilators: Assessment Obtain complete health history including allergies and drug history Assess symptoms related to respiratory insufficiency including breath sounds Obtain vital signs and pulmonary function test data to establish baseline for treatment Planning Provide education regarding drug action, possible adverse effects and precautions Patient to experience improvement in respiratory and pulmonary function Patient to report any adverse effects of drug Interventions Monitor vital signs, respiratory and pulmonary function Monitor patient’s ability to use inhaler and adherence of patient to drug regimen Monitor for adverse effects to drug Maintain an environment as free from triggers for asthma episodes as possible Ensure patient receives adequate fluids (good hydration helps to break up mucous) Ensure patient receives appropriate amounts of vitamins and nutrients (dyspnea can impair absorption of some vitamins and nutrients) if prescribed other inhalers, give bronchodilator first Pharmacotherapy of asthma drugs that can prevent episodes: Several drugs classes are used to prevent asthmatic episodes and for management of chronic asthma Focus is on reducing inflammation Corticosteroids Most effective and most commonly used Mast Cell Stabilizers Leukotriene Modifiers Monoclonal antibodies Coughing: Coughing is means of removing contaminants from lower respiratory tract Cough reflex is triggered by stretch receptors in carina (located at bifurcation of trachea) When stretch receptors are irritated, coughing is initiated by medullary centre Productive coughs are beneficial while non-productive coughs can be very disruptive Antitussives: Antitussives are used to manage non-productive costs Two classes of antitussives are used Opioids (ie codeine) Raise the cough threshold in CNS More effective than non-opioids; used for severe coughs Non-opioids Dextromethorphan Dextromethorphan Trade names Koffex DM, Robitussin DM Therapeutic effects Treating non-productive cough Mechanism of action Raises the cough threshold in the CNS Adverse effects At moderate dose, dizziness, sedation Serous adverse effects Abuse can cause CNS toxicity Depression Ataxia, slurred speech Stupor Seizure Coma, respiratory depression Expectorants: Used to break down bronchial secretions to support cough reflex Expectorants (ex, guaifenesin) Reduce thickness or viscosity of bronchial secretions Available OTC in several formulations Chronic obstructive pulmonary disease (COPD): Cigarette smoking causes approximately 90% of non-asthma COPD Two most common forms of COPD Chronic bronchitis Excess mucus produced in lower respiratory tract Emphysema Loss of bronchiolar elasticity and destruction of alveolar walls Pharmacotherapy used to relieve symptoms and avoid complications Drugs to treat COPD similar to those used to treat asthma Mucolytics and expectorants Bronchodilators Anti-inflammatory agents Long-term oxygen therapy prescribed in later stages to decrease mortality Week 3: Regulation of acid secretion: Parietal cells secrete hydrochloric acid through the activity of H+/K+ proton pump Acid secretion is increased by the activity of: Gastrin receptors Histamine 2 receptors (H2 receptors) PNS – acetylcholine receptors Acid secretion is decreased by the activity of: Prostaglandin receptors (PGE2 receptors) Protection from acid secretion: Goblet cells produce mucous which protects the lining of the stomach Mucous production is stimulated by agonists of PGE2 receptors Pancreas secretes bicarbonate ions into duodenum to neutralize acid to protect mucosa Peptic ulcer disease (PUD): Characterized by erosion of mucosal lining of stomach and/or duodenum Etiology H. pylori infection (85% of cases) - Antibotic given to treat this Chronic use of NSAIDs (reduce production of prostaglandins) Zollinger-Ellison Syndrome (ZES) Tumour that secretes gastrin; gastrin promotes acid secretion by parietal cells Gastric ulcers less common than duodenal ulcers Pain often relieved with food, but returns 1 – 3 hours after meal Stress, mediated by the sympathetic nervous system, leads to vasoconstriction of blood vessels to stomach Reduced secretion of mucous and bicarbonate ions Medications worsen PUD: steroids Gastroesophageal reflux disease (GERD): Chronic condition characterized by persistent heartburn due to weakening of lower esophageal sphincter Medications worsen GERD: steroids Symptoms include: Heartburn, chest pain Nausea, belching Dysphagia, early satiety Pharmacotherapy of PUD and GERD: Change lifestyle factors that may be contributing to severity Goals of PUD pharmacotherapy Relieve symptoms Promote healing Prevent complications Prevent future recurrence Eliminate causative factors Drugs that reduce acid secretion H2-receptor antagonists Proton pump inhibitors Anticholinergics Prostaglandins Drugs that neutralize acid Antacids Antibiotics Amoxicillin, clarithromycin, tetracycline, metronidazole Treat bacterial infections Pharmacotherapy with H2-receptor antagonists: Available OTC and by prescription Pharmacokinetic properties Rapid absorption in small intestine 30-minute onset of action Half-life from 1 to 4 hours Antacids diminish the absorption of H2-receptor antagonists Ranitidine (Zantac) Therapeutic effects and uses Duodenal ulcers, gastric ulcers Hypersecretory conditions (ie ZES) Heartburn, GERD Used off-label to counter medications that promote the development of peptic ulcers Mechanisms of action Blocks H2 receptors on the parietal cells in the stomach to decrease acid production Adverse effects Uncommon and transient Serious adverse effects Blood dyscrasias, especially neutropenia and thrombocytopenia Confusion may occur rarely, usually in elderly or with IV dosing High doses may result in gynecomastia, impotence, or loss of libido in men Pharmacotherapy with proton pump inhibitors (PPIs): PPIs H+/K+ pump on parietal cells, reducing acid secretion in the therapy of PUD and GERD Should be taken about 30 minutes before meals No crushing, has to be taken whole Omeprazole (Losec) Therapeutic effects and uses By prescription, approved for short-term, 4- to 8-week therapy of active peptic ulcers OTC, indicated for relief of heartburn Mechanism of action Reduces acid secretion in stomach by irreversibly binding to the H+/K+ pump Adverse effects Headache, nausea, diarrhea, rash, abdominal pain Serious adverse effects Blood dyscrasias Fatigue weakness Pharmacotherapy with antacids: Composed of carbonate, hydroxide and bicarbonate compounds that neutralize stomach acid Calcium carbonate, aluminum carbonate Aluminum hydroxide, magnesium hydroxide Sodium bicarbonate Can affect absorption of drugs, especially those that require an acidic environment Pharmacotherapy with antacids Adverse effects of calcium antacids Constipation, aggravation of kidney stones Milk alkali syndrome – hypercalcemia Adverse effects of aluminum antacids Constipation, hypophosphatemia Adverse effects of sodium anatacids Fluid retention Adverse effects of magnesium antacids Hypermagnesemia (fatigue, dysrhythmias, hypotension) Aluminum hydroxide (amphojel) Therapeutic effects and uses Most effective used in combination with other antiulcer agents for the symptomatic relief of PUD or GERD Mechanism of action Combines with stomach acid to produce aluminum chloride and water, raising the pH of the stomach Adverse effects Constipation At high doses, aluminum products bind with phosphate in GI tract, and long-term use can result in phosphate depletion Pharmacotherapy of H.Pylori infection: Antibiotics usually given with drug that reduces acid secretion (PPI or H2 blocker) Two or more antibiotics usually given at same time to prevent development of resistance to antibiotics Beta-lactamase, macrolides and tetracyclines are used together Miscellaneous drugs used for PUD and GERD: Sucralfate Stimulates mucous, bicarbonate, and prostaglandin Misoprostol Prostaglandin agonist, promotes mucous secretion and inhibition of acid secretion Bismuth compounds Used for dyspepsia, heartburn, and diarrhea Nursing considerations for patients receiving pharmacotherapy for PUD: Assessment Obtain a complete health history allergies and drug history Assess patient for signs of GI bleeding Obtain baseline vital signs, LOC Obtain complete blood count, liver and renal function tests Planning Provide education regarding the action of drug, possible adverse effects, and precautions Have patient report adverse effects including constipation, abdominal pain, drowsiness and dizziness Interventions Monitor use of other drugs to limit drug interactions Monitor patient for adverse effects Monitor patients for signs of GI bleeding, for abdominal pains as a measure of effective therapy Interventions Monitor kidney and liver function Monitor for absorption of vitamin B12 Constipation: More frequent in older adults Can be a symptom of underlying disease Diagnosis requires at least two of the following symptoms. Two or fewer bowel movements per week Lumpy or hard stools at least 25% of the time Straining to pass stools at least 25% of the time Feeling of incomplete evacuation at least 25% of the time Many causes including: Lack of exercise Insufficient diet, lack of dietary fibre Lack of fluid intake Drugs that reduce GI motility Opioids can cause constipation Severe constipation can lead to: Fecal impaction Complete obstruction of bowel Non-pharmacological approaches Regular exercise promotes more regular GI activity Eating a sufficient amount of food to meet requirements of body Healthy diet including insoluble dietary fibre adequate hydration, drinking the recommended amount of water every day Occasional episodes can be resolved quickly with medication Pharmacotherapy with laxatives: Laxatives are drugs that promote evacuation of bowel Classes Bulk-forming (ie psyillium) Fibre that absorbs water, forming bulkier stool that passes more easily Must be taken with lots of water Complication secondary to administration is obstruction to the esophagus Stool softeners (ie docusate) Surfactant that lowers the surface tension of stool allowing more water to enter stool Often given when constipation poses a risk Stimulants (ie bisacodyl) Irritate bowel, promoting peristalsis Can cause diarrhea and cramping Osmotics (ie magnesium hydroxide) Draw water into GI tract Can cause dehydration Psyllium Mucilloid Trade names Metamucil Psyllium Therapeutic effects and uses Occasional constipation Reduction of blood cholesterol with longer use Mechanism of action Absorbs water in bowel forming a bulky stool Bulky stool stimulates defecation reflex Adverse effects Safest laxative if taken as directed with lots of water Mild cramping Diarrhea Serious effects If not taken with adequate water, can cause obstruction of esophagus or intestines Nursing considerations for patients receving laxative therapy: Assessment Obtain complete health history allergies and drug history Assess bowel sounds and bowel elimination history (ensure that patient does not have obstruction) Planning Provide education regarding drug action, possible adverse effects and precautions Patient to experience relief from constipation, or report lack of improvement Patient to report adverse effects including nausea, vomiting, diarrhea, abdominal pain Interventions Monitor frequency, volume and consistency of bowel movements monitor patient’s fluid intake (and ability to swallow) Diarrhea: Increased fluidity of feces when colon does not reabsorb enough water Often secondary to another condition Etiology GI infection Drugs (antibiotics, NSAIDs, orlistat, digoxin) Inflammation of bowel Foods Diseases of SI and pancreas, leading to malabsorption of food Prolonged diarrhea Imbalances in fluid, acid–base, electrolytes Indication for pharmacotherapy Symptom of underlying disorder Prolonged diarrhea can cause: Fluid imbalance pH imbalance Electrolyte imbalance Therapeutic focus is to eliminate primary cause of diarrhea and to manage symptoms through pharmacotherapy If infection is primary cause, then antibiotics will be most effective treatment but can be combined with antidiarrheals Pharmacotherapy of diarrhea: Opioids (most effective) decrease GI motility via mu receptors, providing more time for water absorption Codeine Diphenoxylate with atropine (Lomotil) Loperamide (Imodium; available OTC) Non-opioids Bismuth subsalicylate (Pepto-Bismol) draws fluid out of bowel, anti-inflammatory Psyllium – absorbs water to form bulk Diphenoxylate with atropine (lomotil) Therapeutic effects and uses Moderate to severe diarrhea Mechanism of action Binds mu opioid receptors in GI tract to reduce peristalsis Atropine blocks ACh receptors to reduce peristalsis Combined, this combination provides more time for water to be absorbed from LI Adverse effects Dizziness Lethargy, drowsiness Anticholinergic effects of atropine Nursing considerations for patients receving antidiarrheal therapy: Assessment Obtain a complete health history including allergies and drug history Obtain vital signs, ECG and electrolytes Obtain and evaluate stool culture Assess for presence of dehydration Planning Provide education regarding drug action, possible adverse effects and precautions Patient to experience relief from diarrhea Patient to report any adverse effects including constipation, continued diarrhea, abdominal pain, confusion, dizziness, fever, blood in stool Interventions Monitor frequency, volume and consistency of stool Monitor fluid and electrolyte levels Monitor for anticholinergic effects including dry mouth initiate safety measures to reduce risk of falls Nausea and vomiting: Nausea Unpleasant feeling of need to vomit accompanied by weakness, diaphoresis, dizziness, and hyperproduction of saliva Vomiting (emesis) Stomach contents forced upward into mouth Controlled by the vomiting center of the brain that receives signals from digestive tract, inner ear, chemoreceptor trigger zone, cortex Pathophysiology of nausea and vomiting: Nausea and vomiting are often secondary to another condition Treatment outcomes should focus on removal of the cause whenever feasible Causes Motion sickness Drugs, toxins GI infection Stress, pain Pregnancy Complications from chronic vomiting may include: Dehydration Electrolyte imbalances Significant weight loss Vascular collapse Dehydration Metabolic alkalosis Pharmacotherapy of nausea and vomiting: Anticholinergics (ie scopolamine) Nausea due to motion sickness Antihistamines (ie dimenhydrinate (Gravol)) Nausea due to motion sickness Cause significant drowsiness Serotonin (5HT3) receptor antagonists (ie ondansetron) Chemotherapy-induced nausea and vomiting Phenothiazines (D2 receptor antagonists; ie prochlorperazine) Antineoplastic therapy Cannabinoids Antineoplastic therapy Corticosteroids (ie dexamethasone) Antineoplastic therapy Post-surgical nausea and vomiting Prochlorperazine (Stemetil) Therapeutic effects and uses Anti-psychotic medication Severe nausea and vomiting Mechanism of action Blocks D2 receptors in brain, preventing signaling to the vomiting centre Adverse effects Anticholinergic effects (orthostatic hypo-tension, dry mouth, sedation) Extrapyramidal effects (with longer usage) Week 5: Anxiety: Anxiety is a generalized feeling of worry, fear or uneasiness about a perceived threat Anxiety, as a part of the stress response, is adaptive and can improve performance When anxiety is excessive or irrational, anxiety is maladaptive and can affect normal functioning and promote GI and cardiovascular disorders Types of anxiety disorders: Generalized Anxiety Disorder (GAD) Excessive anxiety that lasts more than 6 months Symptoms include restlessness, fatigue, difficulty focusing, sense of dread, sleep disturbances Sympathetic effects are common as part of stress response Panic Disorder – intense, immediate feelings of fear, impending doom, increased sympathetic effects Phobias – excessive fear related to objects or situations Obsessive Compulsive disorder (OCD) – recurrent, intrusive thoughts or behaviours Post-traumatic stress disorder (PTSD) – anxiety associated with past event Non-pharnacologic treatment of anixety disorders: Many treatment options are available for anxiety disorders aside from drugs Counseling Cognitive-Behavioural therapy Support groups Complementary and Alternative medicines Yoga Biofeedback Meditation Kava, valerian, melatonin Brain areas associated with anxiety disorders: Limbic system: associated with emotion, learning and memory Reticular formation (part of reticualr activating system) Sleep disorders: Insomnia – lack of adequate sleep Sleep-onset insomnia Difficulty falling asleep Sleep-maintenance insomnia Difficulty staying asleep Sleep-offset insomnia Waking up too early Non-restorative sleep Adequate sleep duration but sleepy during day Drugs classes used to treat anxiety and sleep disorders: CNS depressants Benzodiazepines Barbiturates Other agents Zopiclone Buspirone Act on a continuum in terms of effects Anxiolytic – reduce anxiety Sedative – promote relaxation Hypnotic – promote sleep Pharmacotherapy of anxiety and insomnia: Benzodiazepines Therapeutic effects and uses Drugs of choice for Generalized Anxiety disorder (GAD) and Short-term insomnia therapy (up to about 4 weeks) Route of admin Usually enteral Mechanism of action bind GABAA receptor which causes its Cl- channel to open, decreasing excitability of post-synaptic neurons in limbic system Metabolized by liver, excreted by kidneys Adverse effects Drowsiness Sedation Disorientation Ataxia (lack of coordination of skeletal muscles) Blurred vision Can reduce REM sleep stages Tolerance develops with repeated use Dependency can develop as well Decrease time to fall asleep for patients with insomnia, reduce sleep interruptions Interactions Respiratory depression can occur when mixed with other CNS depressants (alcohol, opoids) Antagonized by flumazenil Lorazepam (Ativan) A benzodiazepine Therapeutic effects General Anxiety Disorder (GAD) Anxiolytic, sedative-hypnotic Anti-seizure Pre-anaesthetic Mechanism of action Binds GABAA receptor, causing inhibition of post-synaptic neurons in thalamus, hypothalamus, limbic system Common adverse effects Same as for benzodiazepines in general Drowsiness, sedation, ataxia, blurred vision, disorientation, anterograde amnesia Increased dose can promote sleep and coma Less common adverse effects Hepatotoxicity, alopecia, anaphylaxis, Cardiac changes after rapid IV Paradoxical CNS stimulation Barbiturates: Used less commonly now for anxiety and insomnia compared to benzodiazepines Dependence – both psychological and physiological dependence occur; withdrawal is severe and can be fatal Tolerance develops to CNS effects, but not to respiratory depression Increased dose to achieve therapeutic effect can be high enough to stop breathing Cross-tolerance – tolerance to barbiturates can promote tolerance to opioids and other CNS depressants Interactions Increase the activity of some liver enzymes which can alter metabolism of other drugs Barbuturates Therapeutic effects Used as anti-seizure, iv anaesthetic Mechanism of action same as for benzo-diazepines; bind GABAA receptors causing opening of its Cl- channels adverse effects Similar to those of benzodiazepines Respiratory depression Paradoxical excitement Convulsions, seizures, and epilepsy: Convulsions Involuntary, violent spasms of large skeletal muscles of face, neck, arms, and legs All convulsions are seizures but not all seizures are convulsions Seizures Disturbance of the brain's electrical activity that may affect consciousness, motor activity and sensation Seizures Causes: infectious diseases, trauma, neoplasms, metabolic disorders (hypoglycemica, electrolyte imbalances), vascular disease (stroke), febrile, certain medications, idiopathic, secondary to another condition Seizures occur when “seizure threshold” is exceeded Epilepsy Any disorder in which patient experiences recurrent seizures Patients with epilepsy tend to have lower seizure thresholds than others More than 50% of cases are idiopathic Divided into categories based on symptoms, distribution of abnormal activity in brain (generalized onset vs partial onset) Classification of seizure disorders: Generalized Onset seizures Multiple foci that spread abnormal neuronal discharges across both hemispheres of the brain simultaneously Four types Tonic-clonic (motor) Aura, intense muscle contraction, loss of consciousness Absence (non-motor) Staring, transient loss of consciousness Atonic (motor) Short duration, characterized by patient stumbling or falling, no loss of consciousness Myoclonic (motor) Contraction of major muscles, jerky motion, no loss of consciousness Classification of seizure disorders: Partial (focal) Onset seizures Usually occur in limited portion of brain symptoms may vary depending on part of brain affected Two types Simple (focal aware) Regional symptoms Motor – can be tonic, clonic, atonic or repeated motions Non-motor – autonomic, behavioural, cognitive, sensory, emotional changes Complex (focal impaired awareness) Altered level of consciousness, often with aura May be motor, sensory and autonomic symptoms Drugs used to treat seizures and epilepsy: Choice dependent on many factors Type of seizure, medical history, results of EEG and other diagnostic tests Four mechanisms of action increasing the stimulation of GABA receptors Reduce Na+ influx into neurons Reduce Ca+2 influx into neurons Block glutamate receptors Drugs that stimulate GABA receptors: Barbiturates (ie pentobarb, phenobarb) indicated primarily for tonic-clonic seizures, but also used as sedative, hypnotic and general anaesthetic purposes Benzodiazepines (ie diazepam, lorazepam) Indicated primarily for absence and myoclonic seizures but also used as anxiolytic and sedative Often used in combination with other drugs Gabapentin – indicated for partial seizures Nursing considerations with drugs that stimulate GABA receptors: Assessment Obtain a complete health history including allergies and drug history Assess neurological status, including recent seizure activity, factors contributing to seizure activity (ie poor nutrition) Planning Reduce the frequency and severity of seizures Provide education to client regarding drug action, possible adverse effects, adherence Interventions Monitor vital signs, especially blood pressure and respiratory rate Monitor neurological status, especially level of consciousness Monitor for signs of renal and liver toxicity Monitor children for paradoxical response (hyperactivity) Monitor for signs of vitamin deficiency (D, B12 and folate) Instruct client to report the following Signs of impending seizure (aura, lethargy, stupor, visual changes) Dizziness, drowsiness Signs of toxicity (nausea, vomiting, diarrhea, rash, abdominal pain, jaundice, hematuria) Signs of vitamin deficiency (clotting issues, anemia, joint pain, bone deformities, skin changes) Instruct client to maintain dosage and schedule of administration Phenobarbital (Phenobarb) Therapeutic effects and uses Indicated for most seizure types except absence seizure Anxiolytic, sedative hypnotic Mechanism of action Increases activity of GABAA receptor, reducing excitability of post-synaptic neurons and increasing seizure threshold Adverse effects Drowsiness, sedation, excitation (children), difficulty focusing, confusion, depression, headache Nausea, vomiting, loss of appetite Vitamin deficiencies (D, B12, folate), anemia laryngospasm Risk of dependency Overdose – CNS depression, respiratory depression, coma, death Diazepam (Valium) Therapeutic effects and uses Status epilepticus Prevention of seizures Anti-anxiety, sedative, hypnotic; often used prior to procedure General anaesthetic Mechanisam of action Stimulates GABA receptors in brain, reducing neuronal discharges Adverse effects Drowsiness, fatigue, dizziness Vertigo Ataxia, laryngeal spasms Urinary retention Menstrual irregularities iv delivery – risk of muscle weakness, hypotension, respiratory depression Drugs that reduce Na+ influx: Desensitize Na+ channels thereby delaying the opening of channels and reducing excitability of neurons Hydantoins (ie phenytoin) Indicated for all seizures except absence Phenytoin-like drugs Carbamezapine – indicated for tonic-clonic and partial Valproate – indicated for absence and tonic-clonic; also for bipolar disorder Phenytoin (Dilantin) Therapeutic effects and uses Prophylactic therapy of all seizures except absence Mechanism of action Delays influx of sodium ions in neurons Slows propagation and spread of abnormal discharges Phenytoin has many interactions! Adverse effects Lethargy, drowsiness, dizziness Headache Bradycardia, hypotension Agranulocytosis, leukopenia, thrombocytopenia Gingival hyperplasia (overgrowth of gum tissue) rashes Weight loss hepatotoxicity Nursing considerations for drugs that reduce Na+ influx: Assessment Obtain a complete health history including allergies and drug history Assess neurological status, including recent seizure activity, factors contributing to seizure activity (ie poor nutrition) Planning Reduce the frequency and severity of seizures Provide education to client regarding drug action, possible adverse effects, adherence Implementation Monitor neurological status, especially level of consciousness as sedation is sign of toxicity Monitor effectiveness of drug therapy Monitor for adverse effects, especially hypersensitivity, hepatotoxicity and nephro-toxicity Monitor for signs of gingival hyperplasia, clotting irregularities Monitor GI and nutritional status Monitor nutritional status instruct patient to take medications at dose and schedule prescribed Instruct client to report Changes in oral health GI irregularities Changes in appetite or weight gain Changes in seizure activity Lethargy, confusion, slurred speech, etc Week 5: Overview of the nervous system: Recognizing changes in internal and external environments Processing and integrating the environmental changes that are perceived Reacting to the environmental changes by producing an action or response Two major subdivisions Central nervous system (CNS) Consists of: Brain Spinal cord Peripheral nervous system (PNS) Consists of: Cranial nerves Spinal nerves Two divisions Sympathetic Neurons originate from the thoracic and lumbar spinal cord Activated under stress Fight-or-flight response Parasympathetic Neurons originate from cranial nerves and sacral spinal cord Activated under non-stressful conditions Rest-and-digest response Target Tissue Sympathetic Parasympathetic Brain Increases alertness Pupil Dilates Constricts Salivary glands Decreases secretion Increases secretion Heart Increases HR, contractility Decreases HR Lungs Dilates bronchi, increases RR Constricts bronchi, decreases RR GI Decreases motility and secretions Increases motility and secretions Pancreas Increases release of glucagon Increases secretion of insulin Adrenal medulla Increases epinephrine secretion Blank Urinary Relaxes bladder muscles, decreases urine production Contracts bladder muscles, Increases urine production Sex Organs Inhibits Stimulates Integumentary Increases perspiration Blank Primary neurotransmitters: Two primary ANS neurotransmitters Norepinephrine (NE) Acetylcholine (Ach) Cholinergic receptors (respond to Ach): Nicotinic Found on postganglionic neurons in ANS Promotes sympathetic and parasympathetic effects found at neuromuscular junction of skeletal muscle cells Muscarinic Found on parasympathetic target tissues Promotes parasympathetic effects Alpha and Beta subtypes Found on target tissues of sympathetic nervous system Promotes sympathetic effects Respond to neurotransmitters such as norepinephrine (NE) and epinephrine Neurotransmitter Receptor Receptor Location Selected Effects Ach Nicotinic Postganglionic neurons in both SNS and PNS Mix of sympathetic and parasympathetic effects Muscarinic Target tissues in PNS Constricts pupils, decreases HR, constricts bronchi, increases GI motility and secretions NE Alpha 1 Target tissues in SNS Constricts arterioles, dilates pupils Alpha 2 Decreases tone of SNS Beta 1 Increases HR and force of contraction of heart Beta 2 Dilates bronchi, dilates arterioles to skeletal muscles Control of autonomic functions: Control of the ANS is involuntary but can be influenced by other factors Can be modified by higher brain centers Strong emotions may trigger physiologic change Role of conscious thought in biofeedback therapy Classification and naming of autonomic drugs: Based on actions of the sympathetic and parasympathetic nervous system Stimulation of the sympathetic nervous system: Adrenergics, sympathomimetics, or adrenergic agonists Inhibition of the sympathetic nervous system: Adrenergic antagonists, antiadrenergics, or adrenergic blockers Stimulation of the parasympathetic nervous system: Cholinergics, parasympathomimetics, or muscarinic agonists Inhibition of the parasympathetic nervous system: Anticholinergics, parasympatholytics, or muscarinic blockers Cholinergic and cholinergic blocking agents: Drugs that stimulate the parasympathetic nervous system by stimulating or blocking the effects of acetylcholine at receptor sites Classification and naming of autonomic drugs: Stimulate parasympathetic nervous system Cholinergics, parasympathomimetics, or muscarinic antagonists Inhibit parasympathetic nervous system Anticholinergics, parasympatholytics, or muscarinic blockers Cholinergic receptors: Found in the autonomic nervous system at the ganglia and the neuroeffector junctions Found in the somatic nervous system at the neuromuscular synapses AchE degrades Ach at all receptor sites Action of cholinergic receptor can be affected directly or indirectly Cholinergic agonists: Blank Muscarinic Nicotinic Receptor location Glands, smooth muscle, cardiac muscle Skeletal muscle, autonomic ganglia, brain, adrenal gland* General actions Pupil constriction Decreased accommodation of the eye Increased GI motility Decreased heart rate Decreased blood pressure Increased glandular secretions (salivary, lacrimal, and sweat) Constriction of bronchial smooth muscle Skeletal muscle contraction Initial stimulation of glandular secretion, followed by inhibition Increased heart rate Increased blood pressure Antagonists Atropine, scopolamine Mecamylamine, succinylcholine, tubocurarine Cholinergics: Type Drug Primary Use Direct acting (muscarinic agonists) Pr bethanechol (Duvoid) Increase urination Blank pilocarpine (Salagen) Glaucoma Indirect acting (cholinesterase inhibitors) edrophonium (Tensilon) Diagnosis of myasthenia gravis Blank galantamine (Reminyl) Alzheimer’s disease Blank neostigmine (Prostigmin) Myasthenia gravis, increase urination Parasympathomimetics: Drugs that increase activity of muscarinic receptors, promoting parasympathetic responses Direct acting agents bind muscarinic receptors Indirect acting agents prevent breakdown of Ach in synapse by inhibiting AchE Ach remains in synapse for longer time producing a greater response Clinical Uses for Direct Acting agents Promotion of bladder motility Promotion of GI motility Treatment of glaucoma Benthanechol (Duvoid) Mechanism of action: interacts with muscarinic receptors to cause actions typical of parasympathetic stimulation – detrusor muscle of bladder contracts and expels urine Primary use: increase urination in clients with non-obstructive urinary retention in clients with atony of the bladder Adverse effects: salivation, sweating, abdominal cramping and hypotension Parasympathomimetics: Indirect acting cholinergic agonists Acetylcholinesterase (AchE) inhibitors Nonselective and affect Ach synapses located at autonomic ganglia, muscarinic receptors, neuromuscular junctions, and Ach synapses in the CNS Clinical uses for Indirect Acting Agents Increase motility (peristalsis) in GI tract Increase motility of urinary tract Some can decrease intraocular pressure Non-autonomic indications for AchE inhibitors: Alzheimer’s Disease (AD) Related to reduction of Ach in cortex AchE inhibitor increases Ach in synapses Reduction of Intraocular Pressure Myasthenia Gravis Donepezil (Apricept) Mechanism of actions prevents breakdown of acetylcholine; enhance transmission in neurons; prolongs the action of Ach Primary use improves memory in people with Alzheimer’s Disease Adverse effects nausea/vomiting, diarrhea, darkened urine, headache, muscle fatigue, muscle cramps Nursing considerations with cholinergic agonists: Assessment Obtain complete history including vital signs with particular consideration of signs related to drug indication Assess for contraindications (GI obstruction, urinary obstruction) Obtain baseline data for planning, implementation and evaluation of treatment Planning Defining appropriate goals for patient (ie improved bowel motility) related to drug treatment Implementation Monitor for adverse effects Direct acting – urinary input / output Indirect acting – muscle weakness Cholinergic – blurred vision, abdominal cramping, diarrhea, difficulty breathing Provide client with instructions for taking medication Provide client with education regarding important adverse effects Evaluation Did treatment achieve goals set out in planning phase Anticholinergics: Produce sympathetic effects by blocking parasympathetic receptors Dilation of the pupils increased heart rate Drying of secretions Decreased GI motility and secretions Bronchodilation Clinical applications of anticholinergics: GI system reduces acid production and GI motility Ophthalmic Dilates pupils Anaesthesia Adjunct decreases secretions Prevents bradycardia Asthma bronchodilates Relatively high incidence of adverse effects Blocking muscarinic receptors leads to predomination of sympathetic effects Tachycardia Dry mouth Dilated pupils Urinary retention Xerostomia leading to hyperthermia Atropine (Atropen) Mechanism of action inhibit parasympathetic nervous system, induces fight or flight response Primary use antidote to cholinergic toxicity, increase heart rate, dilation during eye exams Adverse effects dry mouth, constipation, urinary retention, and tachycardia Contraindication glaucoma Oxybutynin (Ditropan) Mechanism of action relaxes bladder smooth muscle Primary use indicated for the relief of the symptoms of urge incontinence, urgency and frequency in patients with overactive bladder Adverse effects dry mouth, constipation and blurred vision Nursing considerations for cholinergic antagonists: Assessment Obtain thorough history including vital signs, baseline assessment of bowel and bladder function Assess for contraindications Acute angle glaucoma Hypertension Hyperthyroidism Renal conditions Gastroesophageal reflux disorder (GERD) Ulcerative colitis Paralytic ileus Assess for possible interactions Antihistamines enhance muscarinic blockade Some herbal supplements Adrenergic agents and adrenergic blocking agents: Drugs that stimulate the sympathetic nervous system (SNS) by stimulating or blocking the effects of epinephrine, norepinephrine or dopamine in the SNS Adrenergic agents: Induce fight-or-flight response Increase heart rate and force of contraction Dilate pupils Bronchodilate Constrict arterioles Decrease GI motility and secretions Increase blood glucose Decrease urinary tract motility Drug Primary Receptor Subtype Primary Use Salbutamol (sometimes called albuterol) (Ventolin) Beta2 Asthma clonidine (Catapres) Alpha2 in central nervous system (CNS) Hypertension dobutamine (Dobutrex) Beta1 Cardiac stimulant dopamine Alpha1 and beta1 Shock epinephrine (Adrenalin) Alpha and beta Cardiac arrest, asthma formoterol (Foradil) Beta2 Asthma, chronic obstructive pulmonary disease isoproterenol Beta1 and beta2 Asthma, dysrhythmias, heart failure methyldopa Alpha2 in CNS Hypertension norepinephrine (Levophed) Alpha1 and beta1 Shock Pr phenylephrine (Neo-Synephrine) Alpha Nasal congestion pseudoephedrine (Sudafed) Alpha and beta Nasal congestion Selective adrenergic agonists: Specific effects depend on which receptor subtypes are stimulated Medications that are selective for a particular receptor subtype tend to be better for some indications as they have fewer adverse effects Nonselective adrenergic agonists: Some sympathomimetics are nonselective and stimulate multiple adrenergic receptor subtypes For some indications like shock, a drug that stimulates both alpha1 and beta1 receptors is preferred to a more selective agent Epineprhine (Adrenaline) Therapeutic effects and uses Anaphylaxis Hypotension Dysrhythmias Severe ventricular dysrhythmias Bradycardia Asystole Severe asthma Mechanism of action Stimulates alpha and beta-adrenergic receptors Increased blood pressure Increased cardiac output Bronchodilation Primary use Anaphylactic reactions Route S/C, IM or IV Adverse effects Hypertension, dysrhythmias, dry mouth, nausea, vomiting, palpitations, blurred vision, headaches Nursing considerations for Adrenergic agonists: Assessment Obtain complete health history including vital signs, urinary output, heart function Assess for baseline measures of signs and symptoms that should be addressed by medication assess for contraindications and potential drug interactions Planning Appropriate patient education and goal Appropriate education and goal setting with patient Implementation Monitor for potential adverse effects and drug interactions Adverse effects are typically sympathetic in nature Educate client regarding possible adverse effects and when to be concerned Report shortness of breath, palpitations, chest pain Evaluation Did drug therapy achieve patient goals? Adrenergic antagonists: Also called sympatholytics, blockers Mechanism of Action Direct – compete for adrenergic receptor binding sites Types of Adrenergic Antagonists Alpha antagonists / blockers Beta antagonists / blockers Induce cholinergic-like responses by shifting balance to parasympathetic side Actions Decrease heart rate and force of contraction Constrict pupils Bronchoconstrict Dilate arterioles Increase GI motility May be therapeutic or adverse depending on patient's condition Compete with norepinephrine for adrenergic receptors Block NE from reaching receptors Symptoms of fight-or-flight response prevented Impulses from parasympathetic system predominate Adrenergic antagonists and cholinergic agonists produce same symptoms Adrenergic antagonists: Drug Primary Receptor Subtype Primary Use acebutolol (Rhotral, Sectral) Beta1 Hypertension, dysrhythmias, angina atenolol (Tenormin) Beta1 Hypertension, angina carvedilol (Coreg) Alpha1, beta1, and beta2 Hypertension doxazosin (Cardura) Alpha1 Hypertension metoprolol (Lopresor) Beta1 Hypertension nadolol (Corgard) Beta1 and beta2 Hypertension phentolamine Alpha Severe hypertension Pr prazosin (Minipress) Alpha1 Hypertension propranolol (Inderal) Beta1 and beta2 Hypertension, dysrhythmias, heart failure sotalol (Rylosol) Beta1 and beta2 Dysrhythmias terazosin (Hytrin) Alpha1 Hypertension timolol Beta1 and beta2 Hypertension, angina, glaucoma Alpha-adrenergic antagonists: Used in the treatment of hypertension to lower BP Used in the treatment of benign prostatic hypertrophy (increase urine flow) Most common side effect is orthostatic hypotension First-dose phenomenon When sympathetic nervous system blocked, parasympathetic predominates. Hypotension, orthostatic hypotension Decreased blood flow to the brain Syncope Prevented by using lower dose for initial therapy Prevented by giving first dose at bedtime Reflex tachycardia and reflex nasal congestion can also occur Nonselective Block both alpha1 and alpha2 receptors High incidence of side effects like hypotension with reflex tachycardia, nausea, vomiting, and diarrhea Beta1-adrenergic antagonists: Selective (eg. Atenolol, metoprolol) Fewer noncardiac side effects Little effect on bronchial smooth muscle Can be safely given to clients with asthma and COPD Nonselective (ie propranolol) Block beta1 and beta2 receptors Produce more side effects than selective beta1 antagonists Serious side effect is bronchoconstriction. Caution in patients with COPD or asthma Adverse effects Beta blockers also decrease amount of free fatty acids available during metabolic stress. Overdoses potentially serious Maintain or restore cardiovascular function Rebound cardiac excitation may occur if beta blockers withdrawn abruptly. Nursing considerations for adrenegeric antagonists: Assessment Obtain complete health history, vital signs, urinary output and cardiac output Assess for contraindications and drug interactions Planning Identify goals of drug therapy Provide appropriate patient education Implementation Monitor for first-dose phenomenon / syncope Monitor BP, level of consciousness, light-headedness Monitor for possible adverse effects – parasympathetic-like Provide client education regarding timing of taking medication, possible adverse effects and interactions