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Exam 1 Pharm (NURS615) Study Guide
Terms in this set (60)
1. Identify the stages of drug development and how the drugs are tested at each phase.
Phase 1: Testing of a new compound in health subjects, for the purpose of establishing the tolerance of health human subjects at different doses, defining its pharmacological effects at anticipated therapeutic levels, and studying its absorption, distribution, metabolism, and excretion patterns in humans.
Phase 2:Controlled clinical evaluation is done on patients with a specific disease or disorder to determine the medications possible uses and short term risks. Usually the study is conducted on only several hundred subjects or less.
Phase 3: Controlled and uncontrolled clinical trials of a drugs safety and efficacy in hospital and outpatient settings. Gather precise information on drugs efficacy for specific indications to determine if there is a wider range of adverse effects on those that it did in a small study. They try to identify what way the drug is best administered (PO, IV, IM...). If the drug is approved this information forms what goes on the drug label. Phase 3 solidifies phase 2.
Page 33. Pharm 3rd ed.
2. Differentiate between the prescribing of medications by physicians, nurses, and physician's assistants.
Physicians-Their focus is related to pharmacology is on the understanding of biochemistry and prescribing for a given pathophysiology. Their emphasis is on the disease and the drug, with less emphasis on the impact of the patient.
NPs-nurse practitioners prescribed a drug free given pathophysiology, their nursing background leads them to place equal emphasis on understanding the impact the drug will have on the patient. Patient education is a central focus of an NPs practice.
PAs-The focus of the PA's practice is similar to that of the physician.
p.7-8 Pharm 3rd Ed.
3. What factors are associated with clinical judgment when prescribing medications?
Is there a clear indication for drug therapy? What drugs are effective in treating this disorder? What is the goal of therapy with this drug? Under what conditions is it determined that a drug is not meeting the goal in a different therapy or drug should be tried? Are there unnecessary duplications with other drugs the patient is already taking? Would an over-the-counter drug be just as useful as a prescription drug? What about the cost? Where is the information to answer these questions?
P.6 Pharm third edition
4. What is the criteria for choosing an effective drug?
1.) Pharmacodynamic factors of a drug must be specific and selective to the target tissues affected by the disease to have the greatest therapeutic effect with the least adverse effects. The relationship between the drugs desired therapeutic effects and it's adverse effects is called it's therapeutic index. Drugs with the low therapeutic index may require close monitoring for toxicity and versus facts, where is drugs with a wide therapeutic index are fairly safe and require less monitoring. Pharmacodynamics means the study of the effects of the drug on the body. 2.) Pharmacokinetic factors. This is how the body reacts to the drug. It is the study and analysis of the time course of the drug in the body. How well are the drugs absorbed and eliminated. 3.) therapeutic factors 4.)safety 5.)Cost 6.) patient factors 7.) adverse drug reactions 8.) Provider factors
p.25-28 Pharm 3rd edition
5. How does hypoalbuminemia affect the process of prescribing?
ANS: Reduced drug dosages may be indicated in these cases.
In a pt with hypoalbuminemia drugs especially antibiotics are unable to bind as needed with albumin which means there is more of the drug free in the plasma then there would be in a pt with a normal albumin level.Drug-plasma protein binding forms a "reservoir" of drug, but only the free (unbound) drug is available to the tissues to exert a therapeutic effect.
This condition appears to be associated with alterations in the degree of protein binding of many highly protein-bound antibacterials, which lead to altered pharmacokinetics and pharmacodynamics, although this topic is infrequently considered in daily clinical practice. The effects of hypoalbuminaemia on pharmacokinetics are driven by the decrease in the extent of antibacterial bound to albumin, which increases the unbound fraction of the drug. Unlike the fraction bound to plasma proteins, the unbound fraction is the only fraction available for distribution and clearance from the plasma (central compartment). Hence, hypoalbuminaemia is likely to increase the apparent total volume of distribution (V(d)) and clearance (CL) of a drug, which would translate to lower antibacterial exposures that might compromise the attainment of pharmacodynamic targets, especially for time-dependent antibacterials. The effect of hypoalbuminaemia on unbound concentrations is also likely to have an important impact on pharmacodynamics, but there is very little information available on this area.
More Background on hypoalbuminemia:
Albumin comprises 75-80% of normal plasma colloid oncotic pressure and 50% of protein content. When plasma proteins, especially albumin, no longer sustain sufficient colloid osmotic pressure to counterbalance hydrostatic pressure, edema develops.
Albumin transports various substances, including bilirubin, fatty acids, metals, ions, hormones, and exogenous drugs. One consequence of hypoalbuminemia is that drugs that are usually protein bound are free in the plasma, allowing for higher drug levels, more rapid hepatic metabolism, or both.
6. What is the Prescription Drug Marketing Act?
The Prescription Drug Marketing Act of 1987 (PDMA) was signed into law by the President on April 22, 1988. The PDMA was enacted (1) to ensure that drug products purchased by consumers are safe and effective, and (2) to avoid the unacceptable risk to American consumers from counterfeit, adulterated, misbranded, subpotent, or expired drugs. The legislation was necessary to increase safeguards in the drug distribution system to prevent the introduction and retail sale of substandard, ineffective, or counterfeit drugs.
7. How will you stay up to date with medication administration and prescribing?
8. What is the role of the FDA?
FDA is responsible for protecting the public health by assuring the safety, efficacy and security of human and veterinary drugs, biological products, medical devices, our nation's food supply, cosmetics, and products that emit radiation.
FDA is also responsible for advancing the public health by helping to speed innovations that make medicines more effective, safer, and more affordable and by helping the public get the accurate, science-based information they need to use medicines and foods to maintain and improve their health. FDA also has responsibility for regulating the manufacturing, marketing and distribution of tobacco products to protect the public health and to reduce tobacco use by minors.
Finally, FDA plays a significant role in the Nation's counterterrorism capability. FDA fulfills this responsibility by ensuring the security of the food supply and by fostering development of medical products to respond to deliberate and naturally emerging public health threats.
9. What is the primary purpose of drug testing?
ANS: patient safety
• Can affect clinical decisions on a patient's substance use that affects other medical conditions.
• Can affect clinical decisions about pharmacotherapy, especially with controlled substances.
• Increases the safety of prescribing medications by identifying the potential for overdose or serious drug interactions.
• Helps clinicians assess patient use of opioids for chronic pain management or compliance with pharmacotherapy for opioid maintenance treatment for opioid use disorders.
• Helps the clinician assess the efficacy of the treatment plan and the current level of care for chronic pain management and substance use disorders (SUDs).
• Prevents dangerous medication interactions during surgery or other medical procedures.
• Aids in screening, assessing, and diagnosing an SUD, although drug testing is not a definitive indication of an SUD.
• Identifies women who are pregnant, or who want to become pregnant, and are using drugs or alcohol.
• Identifies at-risk neonates.
• Monitors abstinence in a patient with a known SUD.
• Verifies, contradicts, or adds to a patient's self-report or family member's report of substance use.
• Identifies a relapse to substance use.
10. How does albumin effect the distribution of medications?
For drugs which are highly bound to plasma protein, this binding has a large influence on the values of pharmacokinetic parameters. In the case of weekly acidic drugs, albumin is the most important binding protein. Albumin is present both in plasma and in interstitial fluid and its distribution between these fluids may vary. For example, the albumin distribution shifts from plasma fluid to interstitial fluid after prolonged bed rest, severe burns, and during pregnancy. Such changes in albumin distribution, as well as the change in the overall amount of albumin in the body, will alter the extent of plasma protein binding of drugs, which in turn may cause a change in pharmacokinetics.
11. What is the drug's half-life?
The half life of a drug is the amount of time it takes to eliminate one-half of the drug from the body. (p. 21)
12. How does the half-life effect the timing of medication administration?
The half life of a drug determines how often a drug is administered. Doubling the dose does not double the half life. (p. 21)
13. What is meant by the onset of action, peak of action, duration of action of medications?
-Onset of action: Time needed for the drug concentration to reach a minimum level within the blood
-Peak of action: blood concentration and intensity of the response at the highest, absorption rates are greater than elimination rates. Time required for max effect to occur after administration
-Duration of action: Time during which blood levels are above the minimum effective concentration and is not affected by the route of administrations (p.13)
14. Explain first pass metabolism.
The metabolism of a part of the administered dose of a drug before it reaches the systemic circulation. (p. 16)
15. What is meant by a synergistic effect?
When the combining of two drugs produces an effect that is greater than the sum of the individual drugs. (p. 21)
16. What is a steady state?
The amount of drug going in is the same as the amount of drug getting taken out. It takes 4-5 half lives for a drug to reach a steady state and 4-5 half lives to be totally eliminated. (p. 21)
17. What is an additive effect?
An effect in which two substances or actions used in combination produce a total effect the same as the sum of the individual effects.
18. What factors affect the drug's absorption?
-Gastric emptying time
-Absorptive surface area (p. 90)
19. Identify drug metabolism and the role of the isoenzymes of the P450 system.
The Cytochrome P450 isoenzymes (CYPs) are superfamily of haemoprotein enzymes found on the membrane of endoplasmic reticulum. They are responsible for catalyzing the metabolism of large number of endogenous and exogenous compounds. CYPs are also known as mixed function oxidases and mono-oxygenases as metabolism of a substrate by a CYP consumes one molecule of molecular oxygen and produces an oxidized substrate and another molecule of oxygen appears in water as byproduct. CYPs are also called polysubstrate mono-oxygenases as one isoenzyme can have multiple substrates., These enzymes are responsible for biotransformation of drugs and are body's defense against xenobiotics along with P-glycoprotein. P-glycoprotein is efflux pump or transporter present in brain capillary endothelial cells, intestinal mucosal, renal and tubular cells, hepatic canalicular cells etc and are responsible for extrusion or efflux of drugs thereby enhancing drug elimination.
Cytochrome P450 isoenzymes are predominantly present in liver but are also found in intestine, lungs, kidneys, brain etc. Biotransformation of drugs by these enzymes render them ionic and more water soluble so that they can be excreted, drawback of this process is limited bioavailability of drugs
Drug-drug interactions have become an important issue in health care. It is now realized that many drug-drug interactions can be explained by alterations in the metabolic enzymes that are present in the liver and other extra-hepatic tissues. Many of the major pharmacokinetic interactions between drugs are due to hepatic cytochrome P450 (P450 or CYP) enzymes being affected by previous administration of other drugs. After coadministration, some drugs act as potent enzyme inducers, whereas others are inhibitors. However, reports of enzyme inhibition are very much more common. Understanding these mechanisms of enzyme inhibition or induction is extremely important in order to give appropriate multiple-drug therapies. In future, it may help to identify individuals at greatest risk of drug interactions and adverse events.
The cytochrome P450 (P450 or CYP) isoenzymes are a group of heme-containing enzymes embedded primarily in the lipid bilayer of the endoplasmic reticulum of hepatocytes, it takes part in the metabolism of many drugs, steroids and carcinogens .
20. What is the efficacy of the drug?
The maximum effects that the drug can achieve. (p. 14)
21. On the drug concentration curve what is the first sign of a therapeutic effect?
The first sign of therapeutic effect on on the drug concentration curve is the minimal effect concentration. No measurable effect will occur until a minimum effect concentration of free molecules in the body is reached. (p. 13)
22. What is the purpose of a peak and trough level?
To adequately evaluate the appropriate dosage levels of many drugs, the collection and testing of specimens for trough and peak levels is necessary. The trough level is the lowest concentration in the patient's bloodstream, therefore, the specimen should be collected just prior to administration of the drug. The peak level is the highest concentration of a drug in the patient's bloodstream.
serum samples collected to determine the level of an antibiotic or other pharmaceutic agent in the blood. Peak specimens, which represent the highest level, are generally collected ½ hour after the dose is given intravenously or 1 hour after it is given intramuscularly. Trough specimens, representing the lowest level, are generally collected approximately ½ hour before the next dose
23. What is the minimum toxic concentration?
The ultimate aim of drug therapy is to achieve efficacy without toxicity. This involves achieving a plasma concentration (Cp) within the 'therapeutic window', i.e. above the minimal effective concentration (MEC), but below the minimal toxic concentration (MTC).
Quantity at which a solid, water-insoluble substance produces harmful effects in a specified test specie over a stated exposure period.
Read more: http://www.businessdictionary.com/definition/toxic-dose.html#ixzz2sLJi20ce
24. Describe the blood brain barrier and the fetal placental barrier.
-The blood brain barrier refers to a network of capillary endothelial cells in the brain that are impermeable to water soluble drugs. Usually only medications that are lipid soluble cross this barrier.
-The placental barrier is a lipid membrane that allows passage of drugs by simple diffusion. The fetus is generally exposed to the same drug concentrations as the mother. Some drugs may have teratogenic effects causing physical defects in the developing fetus. (p. 18)
25. What is the difference in distribution for each medication route?
Oral must go through the first pass rectal less as well as sublingual. IV bypasses
26. How will renal insufficiency affect drug elimination?
...The metabolism and excretion of many drugs and their pharmacologically active metabolites depend on normal renal function. Accumulation and toxicity can develop rapidly if dosages are not adjusted in patients with impaired renal function. In addition, many drugs that are not dependent on the kidneys for elimination may exert untoward effects in the uremic milieu of advanced renal disease. A familiarity with basic pharmacologic principles and a systematic approach are necessary when adjusting drug dosages in patients with abnormal kidney function. The distinct steps involve calculating the patient's glomerular filtration rate, choosing and administering a loading dose, determining a maintenance dose, and a decision regarding monitoring of drug concentrations. If done properly, therapy in renal patients should achieve the desired pharmacologic effects while avoiding drug toxicity. Physicians must not oversimplify the pharmacologic complexities presented by patients with renal failure by relying excessively on nomograms and "cookbook" equations. In addition to a reduced glomerular filtration rate, patients with renal disease often have alterations in pharmacokinetics such as bioavailability, protein binding, hepatic biotransformation, and volume of distribution. An awareness of biologically active or toxic metabolites of parent compounds that accumulate when the glomerular filtration rate is reduced is also necessary to avoid toxicity. The effects of dialysis on drug elimination and the need for supplemental dosing are additional considerations in patients undergoing renal replacement therapy.
27. What is an additive effect?
refer to number 17?
28. What is a synergistic effect?
Synergistic is the capacity of two or more drugs acting together so that the total effect of these drugs is greater than the sum of the effects if taken independently.
29. What is an antagonistic effect?
The effect produced by the contrasting actions of two (or more) chemical groups
An example of antagonistic effect is the effect between the opposing actions of insulin and glucagon to blood sugar level. While insulin lowers blood sugar glucagon raises it. Thus, regulating the major physiological function of these two chemicals is crucial in order to keep up a healthy level of glucose in blood.
30. Describe the drug effects based on the route of administration.
Oral- Active drugs have to dissolve in liquid and be available in solution as body can't absorb solids. Passive diffusion includes simple diffusion, convective absorption and carrier mediated diffusion, requires no energy expenditure, and can be described as drug movement from an area of high concentration to an area of lower drug concentration. Parental- few absorption problems, IV in injected direcly into venous circulation and begins distribution immediately. IM and SC are affected by the blood flow at the injection sites. (p. 15-16)
31. Describe the role of the isoenzymes.
Isozymes (also known as isoenzymes or more generally as Multiple forms of enzymes) are enzymes that differ in amino acid sequence but catalyze the same chemical reaction. Main players in the p450
32. According to the WHO what is the first step in the prescribing process.
To define the patients problem
33. What is approved by the FDA?
The FDA has decided the benefits of the approved item outweigh the potential risks for the item's planned use.
34. What is off label prescribing?
Off-label use is the use of pharmaceutical drugs for an unapproved indication or in an unapproved age group, unapproved dosage, or unapproved form of administration. Both prescription drugs and over-the-counter drugs (OTCs) can be used in off-label ways, although most study of off-label use centers on prescription drugs. Off-label use is generally legal unless it violates specific ethical guidelines or safety regulations, but it does carry health risks and differences in legal liability
35. What factors place an infant and child at risk when prescribing medications?
The infant and child are an increased risk due to a lack of clinical drug trials, which contributes to decreased information on efficacy, adverse effects, dosage, and frequency. Additionally, medications are often prescribed off-label in children and infants. Children and infants have an immature live and kidney function, which places them at an increased risk for developing adverse effects. (p. 46)
36. What adverse drug reactions (ADRs) is the elderly client at risk for developing?
Polypharmacy increases drug to drug interactions. Hypnotics depressants sedatives; reduced renal clearance, increased risk of confusion. Reduced lean muscle increased fat, reduced eyesight makes overdose a concern, compliance, multiple medical issues.
37. What are the components of each of the Adverse Drug Reactions related to special populations?
38. What are each of the adverse drug reactions? Provide an example of each one. (Anaphylaxis)
Result of an unwanted but normal pharmacological action of a drug given in the usual therapeutic dose
-ex: Bleeding with anticoagulants
Allergic or idiosyncratic effects that are not dose dependent or expected from the pharmacological actions
-ex: Anaphylactic reactions
Cumulative effects of a drug seen with chronic use of medications and are dose and time related
-ex: Supression of hypothalamic-pituitary-adrenal axis with chronic corticosteroid therapy
Delayed adverse drug reactions be come apparent some time after the medication is administered
-ex: Carcinogenesis, Teratogenesis
Seen at the end of drug therapy with a physiological withdrawal after the medication is discontinued
-ex: Withdrawal symptoms seen with amphetamines
Unexpected failure of therapy, most commonly from a drug-drug interaction
-ex:oral contraceptive failure from drug interactions
39. Which medications interact with St. John's Wort?
St. John's Wort interacts with MAO inhibitors, tricyclic antidepressants, serotonin reuptake inhibitors, OTC cold and flu medications, narcotics, and sympathomimetics. (p. 112)
UGT (Uridine 5'-diphospho-glucuronosyltransferase) substrates: St. John's wort modulates UGT enzymes in vitro and may increase the side effects of drugs such as acetaminophen (31).
P-gp substrates: St. John's wort induces intestinal P-gp, resulting in decreased absorption and lowered plasma concentrations of certain drugs including digoxin (54), talinolol (55), and fexofenadine (56). It may also produce severe adverse effects in conjunction with pegylated interferon α (48).
CYP450 3A4 (57) and CYP 2C9 (58) substrates: St. John's wort induces these isoenzymes, affecting the metabolism of certain medications and reducing serum concentrations (59). Drugs metabolized by these enzymes include:
HIV protease inhibitors: Blood levels of indinavir and ritonavir can be significantly reduced, resulting in increased HIV viral load and development of viral resistance (60) (61).
HIV non-nucleoside reverse transcriptase inhibitors: Increased oral clearance and lowered plasma concentrations of nevirapine possibly resulting in antiretroviral resistance and treatment failure (62).
Cyclosporin / Tacrolimus: Blood levels of cyclosporin (45) (46) or tacrolimus (63) (64) can be significantly reduced, resulting in decreased efficacy or acute transplant rejection.
Diltiazem / Nifedipine: Blood levels of diltiazem or nifedipine can be reduced, resulting in decreased efficacy (36).
Irinotecan: Due to changes in hepatic metabolism caused by St. John's wort, levels of irinotecan metabolite SN-38 may be lowered by as much as 40% for up to 3 weeks following discontinuation of St. John's wort (37).
Imatinib: Increased clearance (38) (39).
Docetaxel: Subtherapeutic docetaxel concentrations may result when docetaxel is administered to patients who regularly use St. John's wort (65).
Warfarin: May increase or decrease activity when administered concomitantly. Internal normalization ratio should be monitored routinely (66).
Clopidogrel: May enhance clopidogrel-induced platelet inhibition (17).
Triptans: Increased serotonergic effect and possible serotonin syndrome when combined with sumatriptan, naratriptan, rizatriptan, or zolmitriptan (36).
SSRIs: Increased serotonergic effect and possible serotonin syndrome when combined with citalopram, fluoxetine, fluvoxamine, paroxetine, or sertraline (49).
Tricyclic Antidepressants: Increased serotonergic effect and possible serotonin syndrome when combined with nefazodone, amitriptyline, or imipramine. Possible reduction in efficacy of antidepressants due to changes in metabolism (36).
Zolpidem: decreased plasma concentration (67).
Oral Contraceptives: May reduce blood levels resulting in decreased efficacy (i.e., breakthrough bleeding or pregnancy) (43).
Alcohol: May result in increased sedation (36).
Alprazolam: May reduce blood levels, resulting in decreased efficacy (57).
Dextromethorphan: May reduce blood levels, resulting in decreased efficacy (57).
Simvastatin: Increased clearance, resulting in elevated LDL cholesterol (68).
Atorvastatin: Increased clearance, resulting in elevated LDL cholesterol (69).
Rosuvastatin: Reduces efficacy via increased clearance (70).
Oxycodone: Reduces oxycodone plasma concentrations, significantly reducing its effectiveness (71).
Gliclazide: Increased clearance (58).
Clozapine: Reduces plasma level of clozapine (73).
Methotrexate: Increases exposure and toxicity of Methotrexate in rats(74)
40. Which medications interact with ginseng?
May potentiate insulin and oral hypoglycemics. Interacts with MAOIs to cause headache, tremors and mania. (p. 113)
Anything that can increase bleeding.
Insulin and sulfonylureas: Panax ginseng may increase the hypoglycemic effect of insulin and sulfonylureas (5).
Anticoagulants: Panax ginseng may antagonize the effects of anticoagulants (6) (7) (8).
Monoamine oxidase inhibitors (MAOIs): Panax ginseng may cause manic-like symptoms when combined with MAOIs (9).
Imatinib: Panax ginseng may increase risk of hepatotoxicity (24).
Cytochrome P450 (CYP) 3A4 substrates: Certain ginsenosides can induce CYP3A4 and may increase the clearance of substrate drugs (28) (29).
Raltegravir: Elevated plasma levels of raltegravir, an antiretroviral drug, were reported in a patient following concurrent use of raltegravir and ginseng (32).
41. What are the drug reactions with licorice root?
Licorice interacts with antihypertensives, diuretics, corticosteroids, digoxin, loratadine, procainamide, quinidine and spironolactone. (p. 114)
Cardiac glycosides: Licorice may potentiate toxicity (24).
Insulin: Licorice may have a synergistic effect possibly causing hypokalemia and sodium retention with concomitant use (38) .
Anticoagulants: Licorice may increase the metabolism and clearance of warfarin (19).
MAO-inhibitors (MAO-I): Licorice may potentiate activity of MAO-Is (37) (8)
P-Glycoprotein (P-gp) substrates: Licorice inhibited P-gp, resulting in increased intracellular concentration of the chemo agent daunorubicin, which is a substrate of P-gp (34).
Cytochrome P450 substrates: Glycyrrhizin, a major ingredient of licorice, induces CYP3A (39) and CYP2D6 (44), and can affect the intracellular concentration of drugs metabolized by this enzyme.
Cyclosporine: Licorice greatly reduced the oral bioavailability of cyclosporine by activating P-gp and CYP3A4 (46).
Cortisol acetate:Licorice increased cortisol availability in tissues in the hours following oral Cortisone acetate administration (47).
42. What is the role of the NP in caring for patients who take herbal supplements?
Education! Look for potential interactions
43. What ailment generates the greatest use of over the counter medications?
The most common problems likely to be treated with nonprescription, or OTC, medications in order of fre- quency follow:
2. The common cold
3. Muscle aches (e.g., sprains, strains)
4. Dermatologic conditions (e.g., acne, cold sores,
dandruff, dry skin, athlete's foot) 5. Minor wounds
6. Premenstrual and menstrual symptoms
7. Upset stomach
8. Sleeping problems (p. 123-124)
44. How does doxazosin work?
Doxazosin is a selective Alpha1 Antagonist, which block the effects of catecholamines at the postsynaptic alpha1 receptors in vascular smooth muscle and in the smooth muscle of the bladder neck and prostate. (p. 177)
Doxazosin is used alone or in combination with other drugs to treat hypertension Blocks post synaptic alpha 1 receptors causing arterial & venous dilation decreases total peripherial resistance blocks a 1 recptors in prostatic stromal and bladder reducing sympathetic tone & associated BPH symptoms
45. What effect does prazosin (Minipress) produce?
Decrease in peripheral vascular resistance and lowered BP. BP will be lowered in both standing and sitting positions. (p. 177) Prazosin is an alpha 1 antagonist. Alpha 1 antagonists inhibit alpha adrenergic receptors post-synaptically (Medscape,nd.). This inhibition results in arterial venous dilation yielding a reduction in blood pressure.
46. What is the action and effect of beta blockers?
Beta Blockers act by occupying beta receptor sites and competitively preventing occupancy of these sites by catecholamines and other beta agonists. (p. 184)
Block response to beta adrenergic stimulation Beta blockers, also known as beta-adrenergic blocking agents, are a class of drugs that works by blocking the neurotransmitters norepinephrine andepinephrine from binding to receptors. There are three known types of beta receptors, known as beta1 (β1), beta2 (β2) and beta3 (β3).
β1-adrenergic receptors are located commonly in the heart and kidneys.
β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.
β3- adrenergic receptors are located in fat cells.
When the neurotransmitters are prevented from binding to the receptors, it in turn causes the effects of adrenaline (epinephrine) to be blocked. This action allows the heart to relax and beat more slowly thereby reducing the amount of blood that the heart must pump. Over time, this action improves the pumping mechanism of the heart.
47. What are the adverse effects of beta blockers?
Bradycardia, CHF with pulmonary edema, hypotension, fatigue, weakness, dizziness, anxiety, depression, hyperglycemia, hypoglycemia, unstable diabetes, nausea, vomiting, constipation, diarrhea, impotence, decreased libido, bronchospasm, dyspnea, muscle and joint pain, facial swelling, and pruritic rashes. (p. 187)
48. What effect will result with rapid withdrawal of a beta blocker?
Abrupt withdrawal can be life threatening, it can result in severe angina, MI, ventricular arrhythmias, and death. (p. 191)
49. What patient teaching should be provided when prescribing clonidine or any centrally acting adrenergic blocker?
Attenuation or reversal of antihypertensive effect and potentially life-threatening increases in BP may occur. Because of a potential for additive effects, such as bradycardia and AV block, caution is warranted in patients receiving clonidine concomitantly with agents known to affect sinus node function or AV nodal conduction (eg, beta-blockers). If clonidine therapy is discontinued in patients receiving a beta-blocker, withdraw the beta-blocker several days before gradual discontinuation of clonidine.
Agitation, apnea, bradycardia, CNS depression, coma, constricted pupils, decreased or absent reflexes, drowsiness, hypotension, hypothermia, irritability, lethargy, respiratory depression, reversible cardiac conduction defects or dysrhythmias, seizures, vomiting, weakness.
ER tablets may be taken with or without food and should be swallowed whole and never crushed, cut, or chewed.
Inform patients that if the total daily dose of clonidine does not result in equal doses in the morning and at bedtime, the higher of the 2 doses should be taken at bedtime.
Instruct patients not to discontinue therapy without consulting their health care provider. Sudden cessation of clonidine treatment has, in some cases, resulted in symptoms such as nervousness, agitation, headache, and tremor.
Caution patients who wear contact lenses that treatment with clonidine may cause dryness of the eyes.
Advise patients who engage in potentially hazardous activities, such as operating machinery or driving, of a possible sedative effect of clonidine. Also inform them that this sedative effect may be increased by concomitant use of alcohol, barbiturates, or other sedating drugs.
Advise breast-feeding women taking modified-release tablets not to breast-feed.
50. What are the adverse effects of a beta 1 selective blocker?
Adverse effects of beta-adrenergic receptor blocking drugs can be divided into two categories: 1) those that result from known pharmacological consequences of beta-adrenergic receptor blockade; and 2) other reactions that do not appear to result from beta-adrenergic receptor blockade. Adverse effects of the first type include bronchospasm, heart failure, prolonged hypoglycemia, bradycardia, heart block, intermittent claudication, and Raynaud's phenomenon. Neurological reactions include depression, fatigue, and nightmares. It is not yet proven whether the beta 1-selective adrenergic blockers or those with partial agonist activity reduce the overall frequency of adverse reactions seen with propranolol.
51. Why are beta blockers cautiously prescribed to diabetic clients?
Effects on the liver can lead to gluconeogenesis. Beta blocker action on the pancreas result in impaired insulin release that leads to hyperglycemia in type 2 diabetics and may also impair recovery from hypoglycemia in patients with diabetes. Beta 1 selective drugs are less likely to cause these problems (p. 185)
52. Which medication used in the treatment of Alzheimer's Disease is not an anticholinergic agent?
Namenda (memantine) (p166)
53. What are the anticholinesterase agents used to treat?
Anticholinesterase, any of several drugs that prevent destruction of the neurotransmitteracetylcholine by the enzyme acetylcholinesterase within the nervous system. Acetylcholine acts to transmit nerve impulses within the parasympathetic nervous system—i.e., that part of the autonomic nervous system that tends to induce secretion, to contract smooth muscles, and to dilate blood vessels. In preventing the destruction of acetylcholine, anticholinesterase permits high levels of this neurotransmitter to build up at the sites of its action, thus stimulating the parasympathetic nervous system and in turn slowing the heart action, lowering blood pressure, increasing secretion, and inducing contraction of the smooth muscles. Alzheimer's and Myasthenia gravis
54. What effect does nicotine have on the nicotinic receptors?
Nicotine binds steroselectively to ACh receptors in the autonomic ganglia, in the adrenal medulla, at neuromuscular junctions in the brain. (p. 214)
55. What effect is produced with cholinergic blockers?
Effects include reduction of smooth muscle spasms, blockade of vagal impulses to the heart, decreased secretions (e.g., gastric, salivation, bronchial mucus, sweat glands), production of mydriasis and cycloplegia, and various CNS effects. In therapeutic doses, these drugs have little effect on transmission of nerve impulses across ganglia (nicotinic sites) or at the neuromuscular junction. Several anticholinergic drugs abolish or reduce the symptoms of Parkinson's disease, such as tremors and rigidity, and result in sonic improvement in mobility, muscular coordination, and motor performance. These effects may be due to blockade of the effects of acetylcholine in the CNS.
56. How do cholinergic blockers manage extrapyramidal symptoms?
Centrally acting cholinergic blockers are used to treat Parkinson's disease and to counteract the extrapyramidal adverse reactions associated with some psychotropic drugs.
At therapeutic doses, muscarinic blockade produces mild CNS excitation. At higher doses, scopolamine, and to a lesser extent atropine, can produce agitation, hallu- cinations, and delirium.The relative excess of cholinergic activity in parkinsonian tremor and extrapyramidal symptoms association with antipsychotic drugs can be partially corrected by muscarinc blockade, especially if combined with a dopamine precursor. (P.179)
57. What effect do the cholinesterase inhibitors produce?
Indirect stimulation of cholinergic nerves occurs by inhibiting the cholinesterase enzyme, thus permitting a build up of acetylcholine on the nerve receptor sites. As a result, acetylcholine increases in quantity with successive nerve impulses so that large amounts of acetylcholine can accumulate and repetitively stimulate receptors.
Actions on the parasympathetic nervous system, (the parasympathetic branch of the autonomic nervous system) may cause bradycardia,hypotension, hypersecretion, bronchoconstriction, GI tract hypermotility, and decrease intraocular pressure.
Actions on the neuromuscular junction will result in prolonged muscle contraction.
Administration of reversible cholinoesterase inhibitors is contraindicated with those that have urinary retention due to obstruction.
Used with Myathenia gravis, glaucoma, postural thachy c syndrome as an antidote to anticholinergic poisoning, Parkinsons, Alz
58. What are the pharmacokinetic actions of the cholinesterase inhibitors?
Effects noted in 6 weeks, but can take 18 to 24 weeks for noticeable improvement
Plasma concentrations 2/3 lower in smokers
GI side effects common
59. What is scopolamine commonly administered as a preventive medication?
Scopolamine is used as part of preoperative medication to reduce secretions and facilitate induction of anesthesia. (p. 229)
60. Can medications be administered during pregnancy for myasthenia gravis?
Neostigmine and pyridostigmine can be administered only when the benefits outweigh the risks as they are pregnancy category C. The infant may show muscular weakness and uterine irritability is possible. (p. 205)
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