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NU 636 ADVANCED PHARMACOLOGY EXAM HERZING UNI 2024, Exams of Nursing

NU 636 ADVANCED PHARMACOLOGY EXAM HERZING UNI 2024NU 636 ADVANCED PHARMACOLOGY EXAM HERZING UNI 2024NU 636 ADVANCED PHARMACOLOGY EXAM HERZING UNI 2024NU 636 ADVANCED PHARMACOLOGY EXAM HERZING UNI 2024

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2023/2024

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NU 636
Advanced
Pharmacology
COMPLETED EXAM
2024
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NU 636

Advanced

Pharmacology

COMPLETED EXAM

  1. Which of the following statements best describes pharmacokinetics? a) The study of how drugs affect the body b) The study of how the body absorbs, distributes, metabolizes, and excretes drugs c) The study of how drugs interact with each other and with other substances d) The study of how drugs are used to treat, prevent, or diagnose diseases Answer: B. Pharmacokinetics is the study of how the body handles drugs, including absorption, distribution, metabolism, and excretion. Pharmacodynamics is the study of how drugs affect the body, pharmacology is the study of drugs in general, and pharmacotherapeutics is the study of how drugs are used for therapeutic purposes.
  2. What is the difference between a drug's bioavailability and its bioequivalence? a) Bioavailability is the fraction of a drug that reaches the systemic circulation, while bioequivalence is the similarity between two formulations of the same drug in terms of bioavailability and pharmacological effects b) Bioavailability is the extent to which a drug produces its intended effects, while bioequivalence is the equivalence between two formulations of the same drug in terms of safety and efficacy c) Bioavailability is the rate at which a drug is absorbed into the bloodstream, while bioequivalence is the degree to which two formulations of the same drug have the same pharmacokinetic parameters d) Bioavailability is the concentration of a drug in the blood or tissues, while bioequivalence is the interchangeability between two formulations of the same drug in terms of dosage and administration Answer: A. Bioavailability is the fraction of a drug that reaches the systemic circulation after administration, which can be affected by factors such as absorption, first-pass metabolism, and protein binding. Bioequivalence is the similarity between two formulations of the same

aldosterone secretion. d) It stimulates the production of renin, a hormone that activates the renin- angiotensin-aldosterone system (RAAS), and increases blood volume and pressure. Answer: A. Rationale: Lisinopril is an ACE inhibitor that blocks the conversion of angiotensin I to angiotensin II, which is a powerful vasoconstrictor that increases blood pressure and causes damage to the heart and kidneys. By lowering angiotensin II levels, lisinopril reduces the workload on these organs and protects them from further deterioration.

  1. A 25-year-old woman with a history of asthma is experiencing an acute exacerbation of her symptoms. She uses a metered-dose inhaler (MDI) containing albuterol, a type of beta-2 adrenergic agonist, to relieve her bronchospasm. What is the main pharmacodynamic effect of albuterol and what are some possible adverse effects of this drug? a) It activates the beta-2 receptors in the smooth muscle cells of the bronchi, causing bronchodilation and increased airflow. Some possible adverse effects are tachycardia, palpitations, tremors, and nervousness. b) It inhibits the release of histamine and leukotrienes from the mast cells in the airways, reducing inflammation and mucus secretion. Some possible adverse effects are dry mouth, headache, drowsiness, and fatigue. c) It blocks the muscarinic receptors in the parasympathetic nervous system, preventing bronchoconstriction and mucus production. Some possible adverse effects are blurred vision, urinary retention, constipation, and confusion. d) It stimulates the production of cyclic adenosine monophosphate

(cAMP) in the epithelial cells of the airways, enhancing mucociliary clearance and reducing airway resistance. Some possible adverse effects are nausea, vomiting, diarrhea, and hypokalemia. Answer: A. Rationale: Albuterol is a beta-2 adrenergic agonist that mimics the effects of epinephrine on the beta-2 receptors in the lungs. By activating these receptors, albuterol causes relaxation of the bronchial smooth muscle cells and dilation of the airways. This improves airflow and oxygenation in patients with asthma. However, albuterol can also activate beta-1 receptors in the heart, causing increased heart rate and contractility. This can lead to cardiac arrhythmias, palpitations, chest pain, and hypertension. Albuterol can also cause stimulation of the central nervous system (CNS), resulting in tremors, anxiety, insomnia, and nervousness.

  1. A 45-year-old man with a history of depression is prescribed fluoxetine, a type of selective serotonin reuptake inhibitor (SSRI), to improve his mood. What is the main pharmacokinetic property of fluoxetine and what are some implications for its clinical use? a) It has a long half-life of about 4 to 6 days, which means that it takes several weeks to reach steady-state plasma levels and to achieve its full therapeutic effect. b) It has a high first-pass metabolism by the liver enzymes CYP2D6 and CYP3A4, which means that it has a low bioavailability and requires a high oral dose to be effective. c) It has a low protein binding affinity of about 10%, which means that it has a large volume of distribution and can cross the blood-brain barrier easily. d) It has a high potential for drug-drug interactions due to its inhibition of CYP2D6 and CYP3A4 enzymes, which means that it can increase the plasma levels and toxicity of other drugs metabolized by these enzymes. *Answer: D. Rationale: Fluoxetine is an SSRI that blocks the reuptake of serotonin in the synaptic cleft, increasing the availability of serotonin for binding to its receptors. This enhances the neurotransmission of serotonin and improves the mood and cognition of patients with depression. However, fluoxetine also inhibits the activity of CYP2D6 and CYP3A enzymes, which are responsible for the metabolism of many drugs, such

and monitoring of blood counts, liver function tests, and pregnancy status. Methotrexate should also be supplemented with folic acid to reduce its toxicity.*

  1. A 55 - year-old woman with a history of osteoporosis is prescribed alendronate, a type of bisphosphonate drug, to prevent bone loss and fractures. What is the main pharmacological effect of alendronate and what are some instructions that should be given to this patient? a) It binds to hydroxyapatite crystals in bone tissue and inhibits osteoclast activity, reducing bone resorption and increasing bone mineral density. b) It stimulates osteoblast activity and promotes bone formation by increasing the expression of osteocalcin and alkaline phosphatase. c) It mimics the effects of estrogen on bone tissue and prevents bone loss by modulating the activity of receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoprotegerin (OPG). d) It activates vitamin D receptors in bone tissue and enhances calcium absorption from the intestine and renal tubules. *Answer: A. Rationale: Alendronate is a bisphosphonate drug that binds to hydroxyapatite crystals in bone tissue and prevents their dissolution by osteoclasts. Osteoclasts are cells that break down bone tissue and release calcium and phosphate into the bloodstream. By inhibiting osteoclast activity, alendronate reduces bone resorption and preserves bone mass and strength. This reduces the risk of fractures in patients with osteoporosis. However, alendronate can also cause irritation and erosion of the esophagus if not taken properly. Therefore, patients should be instructed to take alendronate on an empty stomach with a full glass of water

PART B:

What is the difference between pharmacokinetics and pharmacodynamics? Explain with an example of adrug that has different pharmacokinetic and pharmacodynamic properties in different populations.

  • Pharmacokinetics is the study of how the body absorbs, distributes, metabolizes, and excretes drugs. Pharmacodynamics is the study of how drugs interact with their targets and produce effects. A drug that has different pharmacokinetic and pharmacodynamic properties in different populations is warfarin, an anticoagulant that prevents blood clots. Warfarin has a narrow therapeutic range, meaning that small changes in its concentration can have significant effects on its efficacy and safety. Warfarin's pharmacokinetics are influenced by genetic factors, such as polymorphisms in the enzymes that metabolize it, as well as environmental factors, such as diet, age, and drug interactions. Warfarin's pharmacodynamics are also influenced by genetic factors, such as polymorphisms in the receptors that mediate its action, as well as environmental factors, such as vitamin K intake, which antagonizes its effect. Therefore, warfarin requires careful monitoring and individualized dosing to achieve optimal outcomes.
  1. What are the advantages and disadvantages of using fixed-dose combinations (FDCs) of drugs? Give anexample of an FDC that is commonly used in clinical practice and explain its rationale.
  • FDCs are formulations that contain two or more drugs in a single dosage form. The advantages of using FDCs include improved adherence, convenience, cost-effectiveness, and synergistic effects. The disadvantages of using FDCs include increased risk of adverse effects, drug interactions, resistance, and reduced flexibility in dosing. An example of an FDC that is commonly used in clinical practice is trimethoprim/sulfamethoxazole (TMP/SMX), an antibiotic that treats urinary tract infections, respiratory infections, and opportunistic infections in immunocompromised patients. The rationale for using TMP/SMXas an

intervention for this ADR is to stop the drug, administer epinephrine and antihistamines, and use alternative antibiotics. Type C ADRs are dose- and time-dependent and occur after prolonged use of a drug. They are usually related to cumulative or chronic effects of the drug on certain organs or systems. They can be prevented or managed by limiting the duration of treatment, monitoring the organ function or biomarkers, or using prophylactic measures. An example of a type C ADR is osteoporosis caused by long-term use of corticosteroids. The intervention for this ADR is to use the lowest effective dose of corticosteroids, monitor bone mineral density (BMD), and supplement calcium and vitamin D. Type D ADRs are dose- and time- independent and occur after a latent period following exposure to a drug. They are usually related to carcinogenic or teratogenic effects of the drug on certain tissues or cells. They can be prevented or managedby avoiding the drug, screening for early detection, or using preventive measures. An example of a type D ADR is liver cancer caused by exposure to aflatoxin, a fungal toxin that contaminates some foods and drugs. The intervention for this ADR is to avoid contaminated foods and drugs, screen for hepatitis B and C infections, and vaccinate against hepatitis B. Type E ADRs are dose- and time-independent and occur after the withdrawal or cessation of a drug. They are usually related to rebound or withdrawal effects of the drug on certain receptors or pathways. They can be prevented or managed by tapering the dose, switching to a longer-acting drug, or using supportive measures. An example of a type E ADR is seizures caused by abrupt discontinuation of benzodiazepines, a class of drugs that enhance the activity of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter. The intervention for this ADR is to gradually reduce the dose of benzodiazepines, switch to a longer-acting benzodiazepine, or use anticonvulsants. Type F ADRs are dose- and time-independent and occur when a drug fails to produce the desired or expected effect. They are usually related to pharmacodynamic or pharmacokinetic factors that reduce the efficacy or potency of the drug. They can be prevented or managed by increasing the dose, changing the route of administration, or using alternative drugs. An example of a type F ADR is treatment failure caused by resistance to antiretroviral drugs, a class of drugs that inhibit the replication of human immunodeficiency virus (HIV). The intervention for this ADR is to increase the dose of antiretroviral drugs, change the regimen, or usenewer drugs.

What is the difference between apoptosis and necrosis? How do they affect the surrounding tissues?

  • Apoptosis is a programmed cell death that occurs in response to various stimuli, such as DNA damage, oxidative stress, or hormonal signals. Necrosis is an uncontrolled cell death that occurs due to severe injury, infection, or inflammation. Apoptosis does not cause inflammation or damage to the surrounding tissues, asthe cell fragments are phagocytosed by macrophages. Necrosis, on the other hand, causes inflammation and tissue damage, as the cell contents leak out and trigger an immune response. . What are the three main types of cellular receptors? Give an example of each and explain how theytransduce signals.
  • The three main types of cellular receptors are ion channel-linked receptors, G protein-coupled receptors, and enzyme-linked receptors. Ion channel-linked receptors are membrane proteins that open or close ion channels in response to ligand binding, allowing ions to flow across the membrane and alter the membrane potential. For example, acetylcholine binds to nicotinic receptors on skeletal muscle cells and opens sodium channels, causing depolarization and muscle contraction. G protein- coupled receptors are membrane proteins that activate or inhibit intracellular G proteins in response to ligand binding, which in turn modulatethe activity of enzymes or ion channels. For example, epinephrine binds to beta-adrenergic receptors on cardiac muscle cells and activates a G protein that stimulates adenylate cyclase, which converts ATP to cAMP, which activates protein kinase A, which phosphorylates calcium channels and increases calcium influx, causing increased heart rate and contractility. Enzyme-linked receptors are membrane proteins that

parent cell. Meiosis is a process of nuclear division that produces four haploid daughter cells that are genetically different from each other and from the parent cell. The maindifferences between mitosis and meiosis are:

  • Mitosis occurs in somatic cells (body cells), while meiosis occurs in germ cells (sex cells).
  • Mitosis involves one round of DNA replication followed by one round of division (PMAT), while meiosis involves one round of DNA replication followed by two rounds of division (PMAT I and PMAT II).
  • Mitosis results in two daughter cells with 46 chromosomes each (2n), while meiosis results in fourdaughter cells with 23 chromosomes each (n).
  • Mitosis maintains the chromosome number across generations, while meiosis reduces the chromosomenumber by half.
  • Mitosis does not involve crossing over or independent assortment of chromosomes, while meiosisinvolves both processes that increase genetic diversity.
  • Mitosis produces genetically identical cells that are clones of the parent cell, while meiosis producesgenetically different cells that are unique combinations of parental genes.

What are telomeres? What is their function and what happens when they shorten?

  • Telomeres are repetitive sequences of DNA at the ends of chromosomes that protect them from degradation and fusion. Their function is to prevent the loss of important genetic information during DNAreplication, as the DNA polymerase cannot replicate the very ends of the linear chromosomes. Telomeres also prevent the chromosomes from being recognized as broken DNA and triggering a DNA damage response. Telomeres shorten with each cell division, as a small amount of DNA is lost at each replication cycle. When telomeres become too short, they can no longer protect the chromosomes and the cell enters a state of senescence (growth arrest) or apoptosis (cell death). Telomere shortening is associated with aging, cancer, and various diseases. What are the main types of mutations that can occur in DNA? How can they affect the protein structure andfunction?
  • The main types of mutations that can occur in DNA are:
  • Substitution: a change in a single nucleotide base, such as A to G or C to T. Substitution can result inthree possible outcomes:
  • Silent mutation: no change in the amino acid sequence of the protein, as the new codon codes for the same amino acid as the original codon. For example, GCA to GCG, both code for alanine. Silent mutation has no effect on the protein structure and function.
  • Missense mutation: a change in the amino acid sequence of the protein, as the new codon codes for a different amino acid than the original codon. For example, GCA to GAA, alanine to glutamic acid. Missensemutation can have a variable effect on the protein structure and function, depending on the location and nature of the amino acid change. It can cause a loss or gain of function, or alter the interactions with other proteins or molecules.
  • Nonsense mutation: a premature termination of the protein synthesis, as the new codon codes for a stopsignal instead of an amino acid. For example, GCA to TAA, alanine to stop. Nonsense mutation usually has a

What are the main differences between selective and non-selective beta blockers? How do they affect thecardiovascular system and the respiratory system?

  • Selective beta blockers block only the beta-1 receptors, which are mainly located in the heart and the kidneys. Non-selective beta blockers block both beta-1 and beta-2 receptors, which are also found in the lungs, blood vessels, and other tissues. Selective beta blockers reduce the heart rate and blood pressure, but have less effect on the bronchi and peripheral blood vessels. Non-selective beta blockers have similar effectson the heart, but also cause bronchoconstriction and peripheral vasoconstriction, which can worsen asthma and peripheral vascular disease. What is the mechanism of action of heparin and warfarin? How are they monitored and reversed in case ofbleeding?
  • Heparin is an anticoagulant that activates antithrombin III, which inhibits the formation of thrombin and other clotting factors. Warfarin is an anticoagulant that inhibits the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X). Heparin is monitored by measuring the activated partial thromboplastin time(aPTT), which should be 1.5 to 2 times the normal value. Warfarin is monitored by measuring the international normalized ratio (INR), which should be 2 to 3 for most indications. Heparin can be reversed by administering protamine sulfate, which binds to heparin and neutralizes its effect. Warfarin can be reversed by administering vitamin K, which restores the synthesis of clotting factors, or fresh frozen plasma, which provides clotting factors. What are the indications and contraindications of aspirin? What are the common adverse effects andinteractions of aspirin?
  • Aspirin is a non-steroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenase (COX) enzymes, which are involved in the synthesis of prostaglandins, thromboxanes, and prostacyclins. Aspirin has anti- inflammatory, analgesic, antipyretic, and antiplatelet effects. Aspirin is indicated for the treatment of mild tomoderate pain, fever, inflammation, rheumatic diseases, and prevention of cardiovascular events. Aspirin is contraindicated in patients with hypersensitivity to NSAIDs, peptic ulcer disease, bleeding disorders, asthma, renal impairment, pregnancy (third trimester), and children (risk of Reye's syndrome). Aspirin can cause gastrointestinal irritation, bleeding, ulceration, allergic reactions, bronchospasm, renal impairment, hepatotoxicity, tinnitus, and metabolic acidosis. Aspirin can interact with other NSAIDs, anticoagulants, corticosteroids, alcohol, angiotensin-converting enzyme inhibitors (ACEIs), diuretics, and uricosurics.

lactamases), altering the target site of the antibiotic (e.g., ribosomal mutations), reducing the uptake or increasing the efflux of the antibiotic (e.g., porin changes), or acquiring genes that encode for resistance factors (e.g., plasmids). Antibiotics can cause adverse effects such as allergic reactions(e.g., rash), superinfections (e.g., candidiasis), gastrointestinal disturbances (e.g., diarrhea), nephrotoxicity (e.g., aminoglycosides), hepatotoxicity (e.g., tetracyclines), ototoxicity (e.g., aminoglycosides), photosensitivity (e.g., tetracyclines), and What are the three main components of a comprehensive health assessment? How would you conduct eachcomponent for a client with diabetes mellitus?

  • The three main components of a comprehensive health assessment are: health history, physicalexamination, and diagnostic tests.
  • Health history: The nurse would ask the client about their medical history, family history, medications, allergies, symptoms, lifestyle, and psychosocial factors related to diabetes mellitus. The nurse would also assess the client's level of knowledge, self-care practices, and adherence to the treatment plan.
  • Physical examination: The nurse would perform a systematic examination of the client's body systems, focusing on the cardiovascular, renal, neurological, and integumentary systems, which are commonly affected by diabetes mellitus. The nurse would also measure the client's vital signs, height, weight, body mass index (BMI), and waist circumference. The nurse would inspect the client's skin for signs of infection,ulceration, or necrosis, especially on the feet and lower extremities. The nurse would palpate the client's peripheral pulses and check for edema, sensation, and reflexes. The nurse would auscultate the client's heartand lung sounds and check for murmurs or crackles. The nurse would also examine the client's eyes for signs of retinopathy or cataracts.
  • Diagnostic tests: The nurse would order and interpret laboratory tests and imaging studies to monitor theclient's blood glucose level, hemoglobin A1c (HbA1c), electrolytes, renal function, lipid profile, urine