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NR565/ NR 565 FINAL EXAM QUESTIONS WITH CORRECT DETAILED ANSWERS || ALREADY GRADED A+ LATEST VERSION

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NR565/ NR 565 FINAL EXAM QUESTIONS WITH CORRECT DETAILED ANSWERS || ALREADY GRADED A+ LATEST VERSION 1. Explain what it means if a drug is an antagonist? - ANSWER An antagonist according to our text is a drug that takes over a receptor without stimulating that receptor. We see the medication blocking the response of an agonist to that receptor. Such as seen in a beta-blocker keeping the adrenergic nerve activity from increasing the heart rate and therefore able to help decrease the heart rate of the patient taking the medication. Antagonists can make the agonist appear less potent. The effect of the antagonist depends on that of the affinity for the receptor and the blood levels noted in the patient (Woo RN phd ARNP CPNP-PC CNL FAANP, Teri Moser et al., 2015). 2. Another example would be naltrexone. This medication is used in patients that want to not relapse in heroin or opioid usage. The medication blocks the receptors for the opioids and does not allow the drugs to connect to the receptors. The problem with this is that it can cause an overdose if there is a relapse (Pharmacological Treatment | Medication Assisted Recovery, n.d.). - ANSWER 3. What the terms efficacy and bioavailability mean? - ANSWER According to Woo & Robinson (2016), efficacy in medicine means the power of producing the maximum effect of a drug (Woo & Robinson, 2016, p. 14). When thinking about efficacy and medication, an example may include hypertension medication and how it lowers blood pressure but can also have an effect on other mechanisms in the body such as heart rate or kidney function. Patients who are prescribed new medication should be monitored closely on how it may affect the patient's outcome. It also states that drugs with higher efficacy can produce more significant effects than lower efficacy drugs (Woo & Robinson, 2016, p.14) Bioavailability refers to the extent of a substance or a drug that becomes available to its intended biological destination in pharmacology. Therefore, bioavailability measures the rate and fraction of the initial dose of a medication that successfully reaches either; the site of action or the bodily fluid territory from which the drug's intended targets have unimpeded access. The text gave an example of and 500mg oral dose of ciprofloxacin that can be substituted for a 400mg IV dose of ciprofloxacin, which makes up about 80% of its oral availability (Woo & Robinson, 2016, p.19). 4. What are potential adverse effects associated with bbs according to the text? What lab abnormalities can occur? - ANSWER According to the text, there are several potential adverse effects for beta blockers (BB's), and the text classifies them according to each body system, which I will outline for discussion purposes here as well. For the CV system, BB's can cause hypotension, bradycardia, and CHF without pulmonary edema. In the respiratory system, BB's may lead to bronchospasm and dyspnea, which is why they are used in precaution for patients with bronchospastic disorders such as asthma (Woo & Robinson, 2016). Fatigue, weakness and dizziness are all CNS effects that may occur secondary to hypotension, and anxiety, depression, drowsiness, nightmares and insomnia may occur in BB's with high CNS penetration, or in older adults (Woo & Robinson, 2016). BB's can also cause instability in blood glucose levels, especially for patients with diabetes due to alterations in carbohydrate metabolism. Changes in GI motility can lead to anorexia, N/V or constipation (Woo & Robinson, 2016). In the GU system, BB's may cause impotence and decreased libido, which can be a reason for medication noncompliance. Less common reactions include myalgias, skin rashes, and facial edema (Woo & Robinson, 2016). Lab abnormalities associated with BB's include elevated uric acid levels, BUN, serum lipoprotein, potassium and triglycerides (Woo & Robinson, 2016). Glucose levels may be increased or decreased, and ANA titers may also be increased (Woo & Robinson, 2020). 5. Why do bbs, and clonidine require tapers when discontinuing them? - ANSWER Abruptly stopping certain medications such as beta-blockers and clonidine without gradually tapering down the dosages can lead to withdrawal syndromes. Discontinuing cardiovascular drugs like propranolol and clonidine can result in rebound hypertension and increases the risk of cardiovascular events. If a patient taking clonidine suddenly stops taking it, his or her blood pressure will spike dangerous and can even cause a stroke (Akram et al., 2020). Other withdrawal symptoms from clonidine can include nervousness, headache, and tremors (Akram et al., 2020). Similarly, suddenly stopping propranolol or other beta-blockers can cause a spike in blood pressure as well as tachycardia that can even lead to chest pain and potentially a heart attack (Akron et al., 2020). 6. What are the effects of stimulation of beta 2 receptors? - ANSWER According to our text, Beta 2 receptors are located in the smooth muscle of the venules, bronchioles, liver, GI & GU systems, eyes, and pancreas. When stimulated, they increase camp, adenylyl cyclase, and activate cardiac G1. The results of stimulation are by system are relaxation of far vision for the eyes, dilation of the arterioles for skeletal muscle, dilation of pulmonary arterioles, dilation of systemic veins, relaxation of bronchial muscle, increased secretion in bronchial glands, decrease in GI motility, gluconeogenesis in the liver, increased secretion of insulin from the pancreas, relaxation of the urinary bladder, and smooth muscle relaxation in the uterus (Woo, & Robinson, 2016). 7. Another concern of bbs is - ANSWER risk of bronchospasm 8. Considering aceis: what labs require monitoring? What can happen to potassium levels? Are they safe for young women who could be pregnant? - ANSWER ACE inhibitors require practitioners to monitor comprehensive metabolic panel (CMP) or basic metabolic panel (BMP) because this medication causes the body to "potentially retain potassium and impair kidneys if used incorrectly" (Raebel, et al., 2007). In pregnant patient it is a category C in the first trimester and D in the following trimesters. According to the Center for Drug Policy (2006) it is only recommended to take this medication while pregnant if the benefit outweighs the risk to the infant. 9. The P2Y12 inhibitors are commonly prescribed anti-platelets in patients that have - ANSWER experienced an MI (especially those who underwent PCI with stenting) or had a CVA. Let's look a little more at clopidogrel as a medication 10.What sets clopidogrel apart from other P2Y12 inhibitors? - ANSWER Clopidogrel is absorbed in the intestine and activated in the liver. For clopidogrel to be activated it requires two oxidative steps. CYP2C19 is a liver enzyme, specifically the cytochrome P450 enzyme, that is heavily responsible for developing Clopidogrel's active metabolite. Genetic polymorphisms of CYP2C19 inhibit Clopidogrel metabolism and activation making it ineffective. Clopidogrel requires the active metabolite from CYP2C19 to be effective in preventing clot formation. Taking PPI decreases the effectiveness of Clopidogrel. P2Y12 inhibitors share a lot of similarities, but clopidogrel does stand apart in one specific way. The effectiveness of clopidogrel is dependent on the CYP2C19 genotype. As stated in my initial post, clopidogrel is metabolized by CYP2C19, making any variation in the gene to lead to alterations in the drug response. These variations can be linked to an increased risk for major adverse cardiovascular events. Unlike clopidogrel, CYP2C19 genotype does not affect other P2Y12 inhibitors, such as prasugrel and ticagrelor. 11.What alternatives are available to clopidogrel? (Hint: I'm only asking about oral medications that can be long-term) - ANSWER Brilinta (ticagrelor) or Effient (prasugrel) are not dependent on CYP2C19 genotype 12.Woo & Robinson refers to some medications requiring pharmacogenetic testing and some only being recommended. Why do you think some are required while some are only recommended? What types of medications are listed in your book as required? Are there any relationships between those medications that would make them easier to remember? - ANSWER Currently, (according to Woo) four drugs are required to have pharmacogenetic testing performed before they are prescribed: cetuximab, trastuzumab, maraviroc, and dasatinib. 13.When two or more medications are prescribed that are highly protein bound, what is the clinical outcome? - ANSWER Drugs bound to plasma proteins cannot interact with their receptor. Unbound drug is available to produce a pharmacological effect. Warfarin is 98% bound to plasma proteins so even if the binding of a second drug to plasma proteins displaces even a small fraction of warfarin, it can have a dramatic increase in the effects of warfarin 14.Statement - ANSWER The areas of healthcare that have most heavily integrated pharmacogenetics into clinical practice are those that work closely with disease states that are rooted in genetic abnormalities. 15.Statement - ANSWER Oncology: This specialty is on the forefront of precision medicine. For example, breast cancer treatment is partially directed by a pharmacogenetics assessment. The HER2 gene leads to the production of HER2 proteins that in healthy breast tissue regulates cell growth, division, and repair. However, if the HER2 gene mutates it can lead to uncontrolled cell replication. These patients can receive targeted therapy to treat their breast cancer (e.g. Trastuzumab, pertuzumab, etc).

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NR565/ NR 565 FINAL EXAM
QUESTIONS WITH CORRECT
DETAILED ANSWERS || ALREADY
GRADED A+ < LATEST VERSION >




1. Explain what it means if a drug is an antagonist? - ANSWER 🗸 An
antagonist according to our text is a drug that takes over a receptor without
stimulating that receptor. We see the medication blocking the response of an
agonist to that receptor. Such as seen in a beta-blocker keeping the
adrenergic nerve activity from increasing the heart rate and therefore able to
help decrease the heart rate of the patient taking the medication. Antagonists
can make the agonist appear less potent. The effect of the antagonist depends
on that of the affinity for the receptor and the blood levels noted in the
patient (Woo RN phd ARNP CPNP-PC CNL FAANP, Teri Moser et al.,
2015).


2. Another example would be naltrexone. This medication is used in patients
that want to not relapse in heroin or opioid usage. The medication blocks the
receptors for the opioids and does not allow the drugs to connect to the
receptors. The problem with this is that it can cause an overdose if there is a
relapse (Pharmacological Treatment | Medication Assisted Recovery, n.d.). -
ANSWER 🗸

,3. What the terms efficacy and bioavailability mean? - ANSWER 🗸 According
to Woo & Robinson (2016), efficacy in medicine means the power of
producing the maximum effect of a drug (Woo & Robinson, 2016, p. 14).
When thinking about efficacy and medication, an example may include
hypertension medication and how it lowers blood pressure but can also have
an effect on other mechanisms in the body such as heart rate or kidney
function. Patients who are prescribed new medication should be monitored
closely on how it may affect the patient's outcome. It also states that drugs
with higher efficacy can produce more significant effects than lower efficacy
drugs (Woo & Robinson, 2016, p.14) Bioavailability refers to the extent of a
substance or a drug that becomes available to its intended biological
destination in pharmacology. Therefore, bioavailability measures the rate
and fraction of the initial dose of a medication that successfully reaches
either; the site of action or the bodily fluid territory from which the drug's
intended targets have unimpeded access. The text gave an example of and
500mg oral dose of ciprofloxacin that can be substituted for a 400mg IV
dose of ciprofloxacin, which makes up about 80% of its oral availability
(Woo & Robinson, 2016, p.19).


4. What are potential adverse effects associated with bbs according to the text?
What lab abnormalities can occur? - ANSWER 🗸 According to the text,
there are several potential adverse effects for beta blockers (BB's), and the
text classifies them according to each body system, which I will outline for
discussion purposes here as well. For the CV system, BB's can cause
hypotension, bradycardia, and CHF without pulmonary edema. In the
respiratory system, BB's may lead to bronchospasm and dyspnea, which is
why they are used in precaution for patients with bronchospastic disorders
such as asthma (Woo & Robinson, 2016). Fatigue, weakness and dizziness
are all CNS effects that may occur secondary to hypotension, and anxiety,
depression, drowsiness, nightmares and insomnia may occur in BB's with
high CNS penetration, or in older adults (Woo & Robinson, 2016). BB's can
also cause instability in blood glucose levels, especially for patients with
diabetes due to alterations in carbohydrate metabolism. Changes in GI
motility can lead to anorexia, N/V or constipation (Woo & Robinson, 2016).
In the GU system, BB's may cause impotence and decreased libido, which

, can be a reason for medication noncompliance. Less common reactions
include myalgias, skin rashes, and facial edema (Woo & Robinson, 2016).
Lab abnormalities associated with BB's include elevated uric acid levels,
BUN, serum lipoprotein, potassium and triglycerides (Woo & Robinson,
2016). Glucose levels may be increased or decreased, and ANA titers may
also be increased (Woo & Robinson, 2020).


5. Why do bbs, and clonidine require tapers when discontinuing them? -
ANSWER 🗸 Abruptly stopping certain medications such as beta-blockers
and clonidine without gradually tapering down the dosages can lead to
withdrawal syndromes. Discontinuing cardiovascular drugs like propranolol
and clonidine can result in rebound hypertension and increases the risk of
cardiovascular events. If a patient taking clonidine suddenly stops taking it,
his or her blood pressure will spike dangerous and can even cause a stroke
(Akram et al., 2020). Other withdrawal symptoms from clonidine can
include nervousness, headache, and tremors (Akram et al., 2020). Similarly,
suddenly stopping propranolol or other beta-blockers can cause a spike in
blood pressure as well as tachycardia that can even lead to chest pain and
potentially a heart attack (Akron et al., 2020).


6. What are the effects of stimulation of beta 2 receptors? - ANSWER 🗸
According to our text, Beta 2 receptors are located in the smooth muscle of
the venules, bronchioles, liver, GI & GU systems, eyes, and pancreas. When
stimulated, they increase camp, adenylyl cyclase, and activate cardiac G1.
The results of stimulation are by system are relaxation of far vision for the
eyes, dilation of the arterioles for skeletal muscle, dilation of pulmonary
arterioles, dilation of systemic veins, relaxation of bronchial muscle,
increased secretion in bronchial glands, decrease in GI motility,
gluconeogenesis in the liver, increased secretion of insulin from the
pancreas, relaxation of the urinary bladder, and smooth muscle relaxation in
the uterus (Woo, & Robinson, 2016).


7. Another concern of bbs is - ANSWER 🗸 risk of bronchospasm

, 8. Considering aceis: what labs require monitoring? What can happen to
potassium levels? Are they safe for young women who could be pregnant? -
ANSWER 🗸 ACE inhibitors require practitioners to monitor comprehensive
metabolic panel (CMP) or basic metabolic panel (BMP) because this
medication causes the body to "potentially retain potassium and impair
kidneys if used incorrectly" (Raebel, et al., 2007). In pregnant patient it is a
category C in the first trimester and D in the following trimesters. According
to the Center for Drug Policy (2006) it is only recommended to take this
medication while pregnant if the benefit outweighs the risk to the infant.


9. The P2Y12 inhibitors are commonly prescribed anti-platelets in patients that
have - ANSWER 🗸 experienced an MI (especially those who underwent
PCI with stenting) or had a CVA. Let's look a little more at clopidogrel as a
medication


10.What sets clopidogrel apart from other P2Y12 inhibitors? - ANSWER 🗸
Clopidogrel is absorbed in the intestine and activated in the liver. For
clopidogrel to be activated it requires two oxidative steps. CYP2C19 is a
liver enzyme, specifically the cytochrome P450 enzyme, that is heavily
responsible for developing Clopidogrel's active metabolite. Genetic
polymorphisms of CYP2C19 inhibit Clopidogrel metabolism and activation
making it ineffective. Clopidogrel requires the active metabolite from
CYP2C19 to be effective in preventing clot formation. Taking PPI decreases
the effectiveness of Clopidogrel. P2Y12 inhibitors share a lot of similarities,
but clopidogrel does stand apart in one specific way. The effectiveness of
clopidogrel is dependent on the CYP2C19 genotype. As stated in my initial
post, clopidogrel is metabolized by CYP2C19, making any variation in the
gene to lead to alterations in the drug response. These variations can be
linked to an increased risk for major adverse cardiovascular events. Unlike
clopidogrel, CYP2C19 genotype does not affect other P2Y12 inhibitors,
such as prasugrel and ticagrelor.

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