Pharmacology Exam 1 Study Set (Weeks 1 - 3) 318Questions and Answers all Answers 100%Corre, Exams of Nursing

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Bioequivalence Definition - CORRECT ANSWERS Pharmaceutical equivalents that display the SAME RATE and EXTENT OF ABSORPTION Means delivering the SAME AMOUNT of ACTIVE DRUG moiety to SITE OF ACTION when GENERIC or INNOVATOR drugs are administered at the same molar dose under SIMILAR CONDITIONS Therapeutic Equivalents Definition - CORRECT ANSWERS Considered equivalent when the GENERIC drugs are PHARMACEUTICAL EQUILVALENTS and show SAME EFFICACY, SAFETY PROFILE as product whose efficacy and safety has been established Pharmaceutical Equivalents Definition - CORRECT ANSWERS Considered equivalents when BOTH AGENTS contain IDENTICAL AMOUNTS of ACTIVE ingredients in the same SALT or ESTER form, ROUTE of administration and possess IDENTICAL disintegration TIMES, and DISSOLUTION rates. Clinical Judgement in Prescribing - 7 Characteristics - CORRECT ANSWERS 1. Clear Indication for drug?

2. Drug effective in treating this disorder?
3. What are the goals of taking drug?
4. What conditions determine drug IS NOT meeting goal and different therapy should be tried?
5. Duplications with other drugs patient already taking?
6. Would over-the-counter drug be as useful?
7. What about cost? Pre-Clinical - Drug Development Phases: - CORRECT ANSWERS Studies in lab (performed on cells, isolated tissues/organs, animals) Designed to provide basic safety, bioavailability, pharmacokinetic, and initial efficacy data Development of suitable formulation for clinical use

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Reproductive toxicology Long-term carcinogenic testing Phase I - Drug Development Phases: - CORRECT ANSWERS Healthy people - Volunteers: used to establish:

1. Biological effects
2. Safe Doses and tolerability
3. Pharmacokinetics
4. Pharmacodynamic effect (B/P, HR, ECG) Phase I Drug Development - How Stopped - CORRECT ANSWERS 1. Trial stopped if half-life too short or too long
5. Trial stopped with significant ECG changes, severe adverse effects
6. Trials START with sub-pharmacological doses that are escalated following multiple doses (if safe)
7. Pre-clinical data available
8. Costs: $500,000-1.5M / drug tested Phase II - Drug Development Phases: - CORRECT ANSWERS 1. Used to treat disease in a SMALL NUMBER of patients.
9. Establish the ability to IMPROVE patient outcomes Test Efficacy and Safety Phase IIa: Drug limited to single/maximal tolerated dose level. 10-100 patients Phase IIb: Follows proof of concept (Phase IIa) - Several dose levels are tested on target population (dose ranging studies) How Progresses to Phase III - Drug Development - CORRECT ANSWERS Depends on:
10. Drug efficacy relative to competitors

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2. Safety profile
3. Probability of technical success and regulatory success
4. Remaining patent life of drug
5. Costs to produce
6. Market share 7 Price
7. Reimbursement Phase III -Drug Development Phases: - CORRECT ANSWERS Minimum of TWO trials; several thousand patients
8. Compare new med to standard therapy
9. Larger number of patients studied in POPULATIONS across the country
10. New drugs have to AS GOOD or BETTER Confirms clinical dose, frequency, and timing of administration Designed to test the hypothesis of efficacy Adverse Effects are collected to assess benefit-risk potential Phase IV - After Market Drug Development - CORRECT ANSWERS 1. Data submitted to regulatory agencies
11. New drug application takes ~15 months to review
12. Process is expedited for oncology and HIV
13. Begins with post-marketing or safety surveillance trials
14. Harmful effects are discovered that can lead to the withdrawal of the drug Surveillance - FDA continues to monitor (broader population use)

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American Physiological Society - CORRECT ANSWERS 1. Translational research = transfers knowledge new/improved methods of preventing, diagnosing, or treating disease. Creates hypothesis

2. Biomarkers = quantitative measures of biological effect; provide links between mechanisms of action and clinical effectiveness
3. Measure changes in biomarkers in both preclinical models and the clinical indicative of the activity of potentially new drug for treating indication Orphan Drug Status - CORRECT ANSWERS 1. Pharmaceuticals to treat rare disease
4. Fast track application (orphan drug act)
5. Disease should affect < 200,000 people
6. Market exclusivity for 7 years
7. Direct guidance from FDA on design of clinical plan
8. Cost of developing not covered by expected sales Drug Responses Graded Definition and Rationale for Grading - CORRECT ANSWERS 1. Biological effects that can be measured CONTINUALLY up to MAXIMUM responding capacity of the biological system
9. Most drug responses are [xx] (e.g. changes in B/P after drug given)
10. When [xx], responses are EASIER to MANAGE clinically Quintal Drug Response - CORRECT ANSWERS 1. Effects are responses that MAY or MAY NOT occur (e.g. seizures, pregnancy, rash, sleep, death, etc.)
11. Prediction of drug DOSES or BLOOD levels that PRODUCE [xx] responses are MORE reliable at POPULATION level ION Channel Receptor Definition - CORRECT ANSWERS 1. Transmits signals across the cell membrane
12. Increase the flow of [xx] and ALTER the electrical potential or separation of charged [xx] across the membrane

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Types of ION Channel Receptors - CORRECT ANSWERS 1. Acetylcholine (Ach) — (nicotinic) - 5 nicotinic sub-units that form [xx] channel

2. GABA (gamma-aminobutyric)
3. Excitatory amino acids Acetylcholine [Ach] - (Nicotinic) Receptor - Action of - CORRECT ANSWERS muscle contraction GABA Receptor - CORRECT ANSWERS The main inhibitory NEUROTRANSMITTER Excitatory Amino Acid Receptors (examples of) - CORRECT ANSWERS 1. Glycine
4. Aspartame,
5. Glutamate G-Protein Receptors - CORRECT ANSWERS 1. Guanine nucleotide regulator proteins
6. Share similar structure (seven regions) of protein span.
7. Create a POCKET where drugs bind
8. End with "TAIL" inside the cell
9. Individual [x]-proteins have general structure and DIFFER in their BINDING site and the intracellular portions that [x] proteins CONTROL after the drug is bound. G-Protein (2nd Messenger) Examples - CORRECT ANSWERS 1. cAMP - cyclic adenosine monophosphate
10. Ca++ phosphoinositide Diacylglycerols G-Protein Phosphorylate - CORRECT ANSWERS [x]-Protein receptor makes INTRACELLULAR parts of receptor AVAILABLE for phosphorylate G-Protein Sub-Units (3 Total) - CORRECT ANSWERS 1. Alpha

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2. Beta
3. Gamma Transmembrane Receptors Definition and Action - CORRECT ANSWERS 1. Consist of Extracellular hormone-binding domain AND an Intracellular ENZYME domain that phosphorylates the amino acid TYROSINE
4. Hormone binds to receptor == enzyme activation sustains effect Transmembrane Receptors for: - CORRECT ANSWERS 1. Insulin
5. Epidermal growth factor
6. Platelet-derived growth factor Intracellular Receptors Definition - CORRECT ANSWERS 1. Regulate gene expressions
7. Lipid-soluble hormones pass through the cell membrane and bind to intracellular receptors Intracellular Receptors - Action once Bound - CORRECT ANSWERS 1. Displaces stabilizing protein
8. Permits receptor to FOLD into it's ACTIVE conformation
9. Receptor MOVES to nucleus
10. In nucleus controls CONSCRIPTION of GENES by binding specific DNA Hormone Receptor Types DNA Hormone Receptors Five Types - CORRECT ANSWERS 1. Corticosteroids
11. Mineralocorticoids
12. Sex steroids
13. Vitamin D
14. Thyroid hormones

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Role of Enzymes at Receptor Sites - CORRECT ANSWERS 1. Bind to substrates

2. Speed up biochemical reactions
3. Drugs can act to stimulate OR inhibit specific [xx] Agonist Definition - CORRECT ANSWERS Drugs that produce RECEPTOR STIMULATION and a CONFORMATIONAL change EVERY TIME they bind Have affinity and efficacy May demonstrate downregulation or desensitization. **Know what the receptor normally does Antagonist Definition - CORRECT ANSWERS 1. Drugs that OCCUPY receptors WITHOUT stimulating them.
4. They produce NO DIRECT response
5. The response occurs from INHIBITING receptor stimulation (e.g., Beta-Blockers at beta-adrenoceptor) Affinity to BIND, no Efficacy (don't create effect) **Know what the receptor normally does Types of Antagonists - CORRECT ANSWERS 1. Competitive Reversible
6. Irreversible
7. Partial Agonists (part agonist - part antagonists) - they stimulate only SOME of the receptors Phase I Metabolism Definition - CORRECT ANSWERS 1. Results in metabolites with Greater or Lesser pharmacological activity
8. Many are Rapidly Eliminated
9. Others go on to next phase reactions

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Are non-synthetic reactions (CYP-450)

1. Oxidation
2. Reduction
3. Hydrolysis Phase II Metabolism Definition - CORRECT ANSWERS 1. Called synthetic or conjugated reactions because drug molecules metabolized
4. Leads to something being Added to the drug to Synthesize New Compound
5. Metabolites are LINKED to highly charged (Polar) molecules
6. Conjugation to charged molecules MAKES metabolites MORE Water Soluble and EASIER to be Excreted by kidneys Are Synthetic reactions

• Glucuronidation CYP P450 Enzyme Metabolism - CORRECT ANSWERS 1. Responsible for metabolism of the largest number of drugs.

2. May vary based on genetics, and age (levels of enzymes different in children based on age)
3. Drugs MAY COMPETE for the same enzyme resulting in change in metabolic rate, if so administer at different times.
4. Drugs may be inducers (makes metabolism faster) or inhibitors (blocks metabolism, more drug available). Grapefruit juice inhibits CYP3A4. Omeprazole is an inducer

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5. Reaction catalyzes the metabolism of a large number of DIVERSE, highly LIPID- soluble drugs and chemicals.
6. CYPs transfer Electrons from Oxidation of drugs to Electron Transport System of the Endoplasmic Reticulum (a cell organelle) Primarily located in endoplasmic reticulum of the liver cells Enzyme Induction - CORRECT ANSWERS Drugs that increase the expression of drug metabolizing enzymes OR due to:
7. Increased enzyme synthesis; or
8. Decreased enzyme degradation Five most important CYP P450 Enzymes (In order of significance) - CORRECT ANSWERS 1. CYP3A
9. CYP2C
10. CYP1A
11. CYP2E
12. CYP2D CPY3A4 - CORRECT ANSWERS 1. Found in liver, GI Tract
13. Responsible for up to 50% of drug metabolism (CYP3A group)
14. Greater possibility that it will interfere with metabolism when many drugs given.
15. Is influenced by food - Grapefruit juice INHIBITS (increase drug level concentrations). Teach patient to avoid grapefruit just to avoid toxicity.
16. Metabolize these classes of drugs: a. - azole antifungals b. some statins (those that inhibit HMG-CoA reductase) & that lower cholesterol. (older statins) c. corticosteroids (prednisone, prednisolone, dexamethasone)

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d. anticonvulsants (carbamazepine) e. calcium channel blockers d. antihistamines e. anticonvulsants f. antimicrobials

4. Significant drug interactions may increase RISK of Toxicity Phenobarbital - CORRECT ANSWERS Example of a drug that acts as an inducer for

• CYP1A
• CYP2A
• CYP2B
• CYP2C
• CYP2C
• CYP3A Erythromycin, Diltiazem - CORRECT ANSWERS Examples of CYP34A inhibitors CYP1A2 - CORRECT ANSWERS Induced (e.g., metabolizes faster) by broccoli, cabbage, cauliflower (cruciferous vegetables) - may lead to therapeutic failure. Also induced by tobacco smoke and charbroiled meat Inhibited (e.g., more drug available, metabolism blocked) by carrots, parsnips, celery, parsley (apiaceous vegetables) Metabolizes:

1. Theophylline CYP2D6 - CORRECT ANSWERS 1. Primarily in liver
2. Required to convert opioids (e.g., codeine) into morphine (ProDrug example)

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Beta-Blockers are substrate Example of Inhibitor (metabolizes faster): Cimetidine, Amiodarone, Labetalol Example of Inducers (more drug available): Carbamazepine, Phenytoin, Phenobarbital, Rifampin If an Alpha 1 Receptors is STIMULATED, what happens? Use G1 protein - CORRECT ANSWERS Vascular & GU smooth muscle contraction (excite or stimulate) Arterioles = vasoconstriction Eyes = dilate Bladder = contraction, urinary retention Liver = Glycogenolysis (glycogen to glucose-1) Kidneys = Decreased Renin Block Receptor = Orthostatic Hypotension, reflex tachycardia (blood vessel relationship) Catecholamines (Adrenergic Agonists) - CORRECT ANSWERS Oral route = ineffective Duration of Action = short CNS penetration = poor Noncatecholamines (Adrenergic Agonists) - CORRECT ANSWERS Oral route = effective Duration of action = long CNS penetration = good

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Epinephrine (Direct Acting Non-Selective Agonist) - CORRECT ANSWERS Stimulates all four types of receptors (Alpha 1, Alpha 2, Beta 1, Beta 2) Sympathetic system neurotransmitter What is Epinephrine used to treat? - CORRECT ANSWERS Treat:

1. Cardiac arrest, cardiogenic shock, severe hypotension How does Epinephrine work (mechanism of action)? - CORRECT ANSWERS Direct acting, non-selective (many receptors) Mechanism of action: A1 = vascular smooth muscle contraction A2 (dec. cAMP) = feedback inhibition of neurotransmitter release B1 (inc. cAMP) = Increase HR & inotropy (contractions) = Cardiac output Increase B/P, HR, contractility, and Cardiac Output Bronchodilation B2 (inc. cAMP) = smooth muscle relaxation: bronchial, vascular What are the side effects of Epinephrine? - CORRECT ANSWERS Precipitate myocardial ischemia or infarction (inc. cardiac work), arrhythmias What are the contraindications of Epinephrine - CORRECT ANSWERS Narrow angle glaucoma. Use with caution in pts with coronary disease What is patient education for Epinephrine (Epi-Pens)? - CORRECT ANSWERS Do not inject in hands or feet, or digits or in vein Injection in buttocks may not provide relief

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Norepinephrine (NE) - CORRECT ANSWERS Stimulate Alpha 1, Alpha 2, and Beta 1 receptors Sympathetic system neurotransmitter What is Norepinephrine used to treat? - CORRECT ANSWERS 1. Blood pressure control - acute hypotensive states

2. Adjunct treatment for cardiac arrest with profound hypotension How does Norepinephrine work? (Mechanism of Action) - CORRECT ANSWERS Stimulate Alpha 1, Alpha 2, and Beta 1 receptors Direct acting; Non-selective Mechanism of action: Amine derived from tyrosine. Lacks methyl group Low doses = Beta 1 effect more pronounced (increased cardiac output) High doses = Alpha 1 effects dominate (vasoconstriction, systemic vascular resistance) What are the side effects of Norepinephrine? - CORRECT ANSWERS Excessive vasoconstriction decreased end-organ perfusion decreased hepatic blood flow pulmonary vascular resistance reflex bradycardia decreased cardiac output. Alpha 1 Receptor locations - CORRECT ANSWERS 1. Radial muscle (eyes) = dilate
3. Salivary glands = secrete K+ and water
4. Arterioles (coronary, skin/mucosa, skeletal muscles, cerebral, pulmonary, renal) = constriction

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4. Veins (systemic) = constriction
5. Bronchial muscles = relaxation
6. Bronchial glands increase secretions
7. GI Motility = decrease
8. GI Sphincters = contraction
9. Liver = Glycogenesis and gluconeogenesis
10. Kidney - Renin secretion = decrease
11. Ureters (mobility/tone) = tone increases, flow decreased
12. Bladder (trigone and sphincter) = contraction
13. Sex Organ (male) ejaculation What do Alpha-1 receptors do to the body? - CORRECT ANSWERS Dilate the eyes Constrict the arterioles and veins Relax the bronchial muscles and increase secretions Decrease GI motility and contract sphincters Contract the bladder Decrease flow in ureters and increase tone Produce glycogen in the liver (glycogenesis/gluconeogenesis) Decrease renin secretion in the kidneys Ejaculation (male sex organ) What is an Alpha 1 Agonist drug? (Key Example) - CORRECT ANSWERS Phenylephrine (Neo-Synephrine) Other examples: Midodrine (ProAmatine) - prodrug (postural hypotension) Eylometazoline (Neo-Synephrine) Tetrahydrozoline (Visine) Naphazoline (Clear Eyes)

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What is Phenylephrine (Neo-Synephrine) used for? - CORRECT ANSWERS Treat: Vasopressor (IV administration only) Nasal decongestant (topically) to secondarily reduces volume of nasal secretions via vascular effects. Mydriatic (pupil dilator) How does Phenylephrine (Neo-Synephrine) work? - CORRECT ANSWERS Direct acting; Selective Alpha 1 Agonist Mechanism of action:

• Contraction of vascular smooth muscle
• Decreases volume of nasal mucosa (vascular effects) Increases systemic vascular resistance
• Increases both systolic/diastolic B/P
• Constriction of pupillary dilator muscle (pupil dilation) Binds with Alpha-1 and ACTIVATES PIP2 cascade (protein kinase C, increases cellular Ca++) Not a catecholamine (not inactivated by COMT) = Long duration of action What are the side effects of Phenylephrine (Neo-Synephrine)? - CORRECT ANSWERS Rebound mucosal swelling (receptor desensitization) from repeated use Extravasation can lead to tissue necrosis What types of drugs are Alpha 1 Antagonists (think suffix) - CORRECT ANSWERS - osin or - sin suffix

1. Prazosin (Minipress)

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2. Doxazosin (Cardura) - dosed 1x/day
3. Terazosin (Hytrin) - dosed 1x/day
4. Tamsulosin (Flowmax) - more A1 effect, little B1 effect. Metabolized by CYP3A (drug-drug interactions likely, like cimetidine)
5. Silodosin (Urorec, Rapaflo) - more A1 effect, little B1 effect
6. Alfuzosin (Uroxatral) - more A1 effect What do you treat with Alpha-1 Antagonist (Blocker) (-osin or -sin suffix) - CORRECT ANSWERS 1. Benign prostate hypertrophy (BPH)
7. Hypertension
8. Raynaud phenomenon (vasospasm can lead to digital ischemia) What is the mechanism of action of Alpha-1 Antagonists (selective) (-osin or -sin suffix) What happens when and Alpha-1 receptor is blocked from being stimulated? - CORRECT ANSWERS 1. Arteriolar and venous vasodilation
9. Inhibits smooth muscle contraction in prostate What are the side effects of a selective Alpha-1 Antagonist (blocker)? (-osin or -sin suffix) What happens when the Alpha-1 Antagonist action EXCEEDS the therapeutic threshold and causes a side effect? - CORRECT ANSWERS Side Effects: Orthostatic hypotension, syncope, dry mouth, nightmares, sexual disfunction, lethargy

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Cautions: If B/P is less than 120/80 - skip the dose 1st dose phenomenon (orthostatic hypotension) Drug-Drug Interactions:

• Alcholol (many of the -osin, -sin drugs) Prozosin = Beta-adrenergic blockers, Clonidine, Indomethacin Tamsulosin = cimetidine Terazosin = NSAIDs, sympathomimetics, estrogens, verapramil How should you educate patients regarding A1 Antagonists (-osin or -sin suffix) - CORRECT ANSWERS - Take as exactly as prescribed, same time of day
• Avoid NSAIDs
• If for BPH, teach s/s of BPH to monitor for
• Lifestyle factors if for HTN (weight, diet) How do Alpha 2 Receptors (G1 protein) work on the body? (think inhibition) - CORRECT ANSWERS Inhibition NE (norepinephrine) release (primarily a CNS response) Presynaptic nerve terminals of smooth muscles Decrease heart rate, blood flow, peripheral resistance, Renal vascular resistance. Platelets = aggregation Lipocytes = inhibit lipolysis Pancreas = decrease insulin

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Alpha 2 Receptors - Organ Locations (all) - CORRECT ANSWERS 1. Skin/mucosa arterioles = constriction

2. Platelets = aggregation
3. Liver = glycogenolysis, and gluconeogenesis 4· Pancreas (islet cells) = decrease secretions (insulin)
4. Fat cells = inhibition lipolysis What are examples of Centrally Acting Alpha-2 Agonists? - CORRECT ANSWERS Clonidine (Catapress) Methyldopa Others mentioned in Chpt 11: Guanabenz Guanfacine What patient education should you give for centrally acting A2 Agonists? - CORRECT ANSWERS - Take as prescribed

• Take missed doses ASAP
• Do not double doses
• These drugs to be withdrawn slowly over 2-3 days (rebound hypertension)
• Proper patch placement
• Lifestyle management for HTN control Methyldopa - interactions with herbs (ask about herbal use) What is Clonidine (Catapress) used to treat? - CORRECT ANSWERS 1. Antihypertensive

2. Opioid withdrawal
3. Antidiarrheal in patients with autonomic neuropathy (increases NaCl and decreases bicarb (HCO3-)

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4. ADHD

How does Clonidine (Catapress) work? - CORRECT ANSWERS Downregulates norepinephrine release. Binds to receptors in CNS (imidazoline receptors) = antihypertensive effect IV dose = vasoconstriction & hypertension followed by hypotension (pre-synaptic response) Oral dose = accumulates in CNS (CV control center) = suppresses sympathetic outflow What are the side effects of Clonidine (Catapress)? What happens when the inhibitory actions (A2-central agonist) exceed the therapeutic threshold and cause a reaction? - CORRECT ANSWERS Abrupt stop = rebound hypertension (taper drug gradually). Dry mouth, sedation, sexual dysfunction. Drug-Drug Interaction:

• Alcohol, antihistamines, phenothiazines, barbiturates, benzodiazepines, Beta- adrenergic blockers, Nitrates, Prozosin, TCAs, Verapramil What is Methyldopa used to treat? - CORRECT ANSWERS Antihypertensive; especially in pregnancy What is the mechanism of action of Methyldopa? - CORRECT ANSWERS Analog of L-dopa. Binds to presynaptic alpha-2 receptors (greater affinity than NE) Causes downregulation of NE release in vasomotor center. Decreases sympathetic outflow from vasomotor centers (decreases blood pressure)

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What are the side effects of Methyldopa? What happens when the inhibitory actions (A2-central agonist) exceed the therapeutic threshold and cause a reaction? - CORRECT ANSWERS Hemolytic anemia - alters RBC surface antigens, hepatotoxicity, edema, impotence, sedation Lactation: inhibition of dopamine in hypothalmus - increases prolactin Drug-Drug Interactions: Alcohol, antihistamines, beta-adrenergic blockers, haloperidol, levodopa, lithium, MOA inhibitors, nitrates, TCAs, Herbals: Licorice, yohimbe, gingseng What is an example of a Selective Alpha 2 Antagonist that has not clinical use, but is used in some herbal preparations? - CORRECT ANSWERS Yohimbine (discontinued in USA) and is in some herbal preparations for erectile dysfunction/weight loss. Other: Idazoxan (Research purposes only) NOTE: Drug-Drug interaction with Methyldopa What drug is an example of an Alpha 1 Agonist that is selective? - CORRECT ANSWERS Oxymetazoline (Afrin-nasal) What is Oxymetazoline (Afrin) used to treat? - CORRECT ANSWERS 1. Nasal congestion

2. Allergic reactions of the eye
3. Rosacea; facial erythema What are the side effects of Oxymetazoline (Afrin)? - CORRECT ANSWERS Increased runny/stuffy nose, blurred vision, tachycardia, headache, dizziness, drowsiness, lightheadedness, high blood pressure, nervousness, trembling, trouble sleeping, weakness

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Repeated use = rebound mucosal swelling (receptor desensitization) How does Oxymetazoline (Afrin) work in the body? - CORRECT ANSWERS Promotes smooth muscle contraction by increasing cellular calcium levels (A1 effect) and Elicits vasoconstriction through inhibition of adenyl cyclase (A2 effect) What type of adrenergic drug is Amphetamine? - CORRECT ANSWERS Indirect Acting Agonist, a RELEASING agent What is Amphetamine used to treat? - CORRECT ANSWERS 1. ADHD

2. CNS stimulant to reduce fatigue, treat depression, narcolepsy
3. Appetite suppressant (obesity) How does Amphetamine work on the body? - CORRECT ANSWERS Causes release of norepinephrine. At high doses releases Dopamine and Serotonin. Increase HR and B/P. Indirect acting What are the side effects of Amphetamine? - CORRECT ANSWERS Dependence, high potential for addition/abuse. Restlessness, anxiety, tremor, hyperreflexia, increased blood pressure, tachyarrhythmias What are the contraindications of Amphetamine? - CORRECT ANSWERS Concurrent MOA inhibitor treatment What type of drug is Cocaine? - CORRECT ANSWERS Indirect Acting Agonist - Uptake Inhibitor

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Is a Prodrug - converted to morphine by CYP2D6 enzyme What is cocaine used to treat? - CORRECT ANSWERS Local anesthetic How does cocaine work on the body? - CORRECT ANSWERS Blocks reuptake of catecholamines

• CNS: general stimulation
• CV small doses (Bradycardia);
• CV moderate doses (tachycardia, vasoconstriction, arrhythmia, MI)
• Local Anesthetic: Blocks Na+ ion channels - reduces nerve fiber conduction -Thermoregulation = pyrogenic What are side effects of cocaine? - CORRECT ANSWERS CV: myocardial ischemia, coronary vasospasm, fatal arrhythmias. High potential for abuse What drug is an example of an indirect acting agonist that is an MOA inhibitor? - CORRECT ANSWERS Selegiline (Deprenyl) What is Selegiline (Deprenyl) used to treat? - CORRECT ANSWERS 1. Parkinsons Disease

2. Major depressive disorder (transdermal patch)
3. ADHD (off-label) How does Selegiline (Deprenyl) work? - CORRECT ANSWERS Selectively metabolizes dopamine. Irreversible inhibitor. What are the side effects of Selegiline (Deprenyl)? - CORRECT ANSWERS Severe: Hypertensive crisis, if eats with food/drink rich in tyramine (smoked or processed meats, fermented foods, soy products).

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Orthostatic hypotension, arrhythmias, hallucinations, extrapyramidal symptoms, sudden sleep episodes, mental status changes Common: xerostomia (dry mouth), constipation (anticholinergic effects). Headaches, dizziness, insomnia, nausea Caution: Do not stop abruptly (antidepressant, anti-parkinsonian discontinuation syndromes) What are the contraindications for Selegiline (Deprenyl)? - CORRECT ANSWERS Do not give within 10 days of elective surgery (blood pressure effects) What education should you give to someone taking Selegiline (Deprenyl) - CORRECT ANSWERS Do not stop abruptly (antidepressant, anti-parkinsonian discontinuation syndromes) Foods rich in thramine (avoid) What is an example drug for a COMT Inhibitor (indirect acting)? - CORRECT ANSWERS Entacapone (Comtan) (used in combination with Levodopa and Sinemet) What is Entacapone (Comtan) used to treat? - CORRECT ANSWERS Parkinsons Disease How does Entacapone (Comtan) work? - CORRECT ANSWERS Inhibitor of catechol o-methyl transferase (COMT), an important enzyme for degradation of Dopamine (biogenic amines) Route: oral What are the side effects of Entacapone (Comtan)? - CORRECT ANSWERS Severe:

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Dyskinesia Orthostatic hypotension Syncope Hallucinations, psychosis Rhabdomyolysis Fibrotic complications Colitis NMS-like symptoms if rapidly discontinued Common: Dyskinesia, Hypo/hyperkinesia N&V and diarrhea, Dyspepsia, flatulence, Constipation Discolored urine Dizziness, Fatigue Hallucinations Back pain Dry mouth Dyspnea Anxiety, agitation, mood changes, confusion, compulsive behaviors Purpura What are two examples of drugs that are non-selective Alpha receptor Antagonists?

• CORRECT ANSWERS Phentolamine (Regitine) - Reversible Phenoxybenzamine (Dibenzyline) - Irreversible What is Phenoxybenzamine (Dibenzyline) used to treat and how does it work? - CORRECT ANSWERS Pheochromocytomas Action:

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Inhibits neuronal and extraneuronal norepinephrine reuptake. Prevents catecholamines from overcoming blockade, last for days until new receptors are generated. What is Phentolamine (Regitine) used for? - CORRECT ANSWERS 1. Antihypertensive (particularly in patients with pheochromocytoma)

2. (less) sympathomimetic amine overdose; including extravasation into soft tissue How does Phentolamine (Regitine) work? - CORRECT ANSWERS Competitive antagonist (non-selective) Causes an alpha receptor blockade and dilates smooth muscles Decreases blood pressure, decreases stroke volume rate What are the side effects of Phentolamine (Regitine)? - CORRECT ANSWERS Orthostatic hypotension Reflex tachycardia and arrhythmias (increased NE release which increases Beta 1 receptor stimulation) What are the contraindications of Phentolamine (Regitine)? - CORRECT ANSWERS Coronary artery disease What route is used for Phentolamine (Regitine)? - CORRECT ANSWERS IM or IV; short duration of action What are two examples of a mixed-acting Agonist? - CORRECT ANSWERS Ephedrine (no real clinical use) Pseudoephedrine (Sudafed) - Nasal mucosa = decrease inflammation, decrease mucous production (OTC med)