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Health, Medicine, Nursing
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English (U.S.)
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Topic:

Bioavailability, Cytochrome P450, and Heparin

Coursework Instructions:

Please answer the questions giving multiple choice or summary writing.
Note: When taking the midterm exam, read each question carefully. The exam questions have only one answer, unless the question specifically states there is more than one correct answer.
1.Understand what a prodrug is, activation/inactivation by liver enzymes, and how it differs from active drugs.
2.Know what bioavailability and pharmacokinetics mean.
3.Bioavailability is affected by chemical instability, solubility, and first-pass metabolism.
4.Bioequivalence does not affect bioavailability.
5.Understand what the Cytochrome P450 system is in the liver.
6.Clopidogrel (Plavix) is a prodrug and must be activated by hepatic CYP2C19 metabolism; individuals who are poor metabolizers may not form the active metabolite and have reduced antiplatelet response.
7.A drug’s half-life determines how often the drug is administered.
8.Steady state of a drug is reached in approximately 4 to 5 times the half-life.
9.Know about inhalation, oral, and parenteral drug action and the onset of their effects.
10.Know the mechanism of action of anticoagulants (e.g., warfarin, apixaban, heparin).
11.Heparin produces rapid anticoagulation by binding with antithrombin III, and inhibits factors IXa, Xa, XIIa, and XIII.
12.Monitor heparin with aPTT (low dose SC heparin [5000 units BID] does not require aPTT monitoring).
13.Warfarin inhibits vitamin K-dependent blood factors II, VII, IX and X; takes several days for its anticoagulant effect.
14.Monitor the International Normalized Ratio (INR) when Warfarin is used.
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15.Blood factor IIa inhibitor (direct thrombin inhibitor): dabigatran (Pradaxa).
16.An antidote to dabigatran-induced hemorrhage is idarucizumab.
17.Blood factor Xa inhibitors: apixaban (Eliquis), edoxaban (Savaysa), rivaroxaban (Xarelto), fondaparinux (Arixtra).
18.Know what pulmonary emboli are, where they come from, and what these emboli do in the body.
19.Know the risk factors for cerebrovascular accident (CVA).
20.Know the elements involved in the action potential of myocardial tissue.
21.Know what tuberculosis is and its epidemiology in the world.
22.Pulmonary TB is often associated with caseous necrosis.
23.Isoniazid (INH) is famous for causing jaundice when combined with other drugs in a multidrug combination for treating TB.
24.Be able to explain the side effects of multidrug therapy/polypharmacy.
25.Know the difference between vertical and horizontal transmission of organisms.
26.Know how empiric antimicrobial therapy is selected.
27.Antibiotic drugs that inhibit cell wall integrity include penicillins, ampicillin, cephalosporins, and carbapenems
28.Antibiotic drugs that inhibit bacterial protein synthesis include the aminoglycoside, tetracyclines, fluoroquinolones and tetracyclines.
29.Fluoroquinolones: Use is reserved for pneumonias or exacerbations of chronic bronchitis to decrease the potential for development of further resistance.
30.Know the differences between endotoxic and exotoxic bacteria.
31.Invasion period is when the immune and inflammatory responses are initiated.
32.Explain the cause of upper and lower respiratory tract infections, especially pneumonia.
33.List the antibiotics that should and should not be used in children.
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34.Be able to discuss antibodies in newborns.
35.Know about B cell maturation.
36.Know the roles of T cell subtypes.
37.Know ABO blood type compatibilities.
38.Understand how cytokines cause fever.
39.Be familiar with the signs/symptoms and therapy for asthma.
40.Know what pathophysiologic factors increase respiratory rate.
41.Know how to interpret an arterial blood gas.
42.Know the ABGs for metabolic acidosis, metabolic alkalosis, respiratory alkalosis, and respiratory acidosis.
43.Know the causes of respiratory acidosis.
44.Be able to explain COPD and stepwise therapy (additions to current COPD medications) in its treatment.
45.Know the cause for infant weight loss in the early postnatal period.
46.Be able to explain hypoxemia at altitude (reduced oxygen inspiration).
47.Discuss how pulmonary arterial hypertension is associated with right ventricular hypertrophy and an enlarged pulmonary artery.
48.Be able to explain fluid and electrolyte disorders.
49.Know the laboratory values of magnesium, calcium, sodium, and potassium.
50.Be able to explain how aldosterone affects sodium and water.
51.Know the mechanism of action of each diuretic class.
52.Know the effects of atrial natriuretic peptide (ANP).
53.Be able to explain the relationship between edema and oncotic pressure.
54.Be able to differentiate corticosteroids by potencies, mechanism of action, and pharmacokinetics.
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55.Be able to explain how angiotensin affects the cardiovascular system.
56.Know the unique pharmacokinetics of amiodarone.
57.Amiodarone can cause thyroid and pulmonary toxicity.
58.Know what drugs are used for angina: beta-adrenergic antagonists (beta-blockers), angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), nitrates, calcium channel blockers (CCBs).
59.Remember that many heart failure patients have more than just heart failure; look for underlying hypertension, angina, etc.
60.Be able to describe how electrolyte serum levels affect digoxin serum levels.
61.Know how hyperkalemia is caused by renal failure and Addison’s disease.
62.Know how to treat hypercalcemia with calcitonin and pamidronate (nitrogen containing bisphosphonate).
63.What is compensatory hyperplasia?
64.What are the effects of nonsteroidal anti-inflammatory drugs (NSAIDs)?
65.An NSAID safe for use in CAD patients is naproxen.
66.NSAIDs can cause GI bleeding (indicated by darkening of stools and epigastric pain); one recommendation is switch to a COX-2 inhibitor (i.e., celecoxib).
67.Corticosteroids include glucocorticoids (e.g., prednisone, prednisolone, dexamethasone, hydrocortisone, methylprednisolone) and mineralocorticoids (e.g., aldosterone).
68.Patients on corticosteroids should be monitored for changes in skin, muscle wasting, blood pressure, weight gain, blood glucose and vitamin D levels, and any vision changes.
69.What are the side effects of diphenhydramine?
70.Understand the advantage of second-generation antihistamines like loratadine.
71.Know how long after ingestion it takes dimenhydrinate (Dramamine) to prevent motion sickness.
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72.Patients with a history of kidney stones should avoid products containing calcium.
73.Know the factors predisposing individuals to antibiotic resistance.
74.Fluoroquinolones have a boxed warning for tendon rupture.
75.Know the predisposing factors for pseudomembranous colitis.
76.Chronic pain is pain not due to cancer or a recognized medical condition lasting more than 3-6 months.

Coursework Sample Content Preview:
Nursing Question
1 Prodrugs are medications that must undergo chemical conversions through metabolic activities such as activation by CYP3A4 hydroxylation in the liver. In contrast, whereas active drugs are the pharmaceutical ingredients that directly function upon absorption. Certain enzymes activate prodrugs.
2 Bioavailability refers to the ability that a drug has regarding its absorption in the body, and pharmacokinetics is the discipline involving the study of time taken by drugs for absorption and distribution within the body.
3 First pass metabolisms involve the presystemic metabolisms where upon entering the life, the drug undergoes extensive biotransformation that drastically reduces its bioavailability. The chemical instability and solubility affect the rate at which the drug absorption in the systemic circulation takes place.
4 With the understanding that bioavailability refers to the rate of an active drug being absorbed into the body and bioequivalence as the similarity between drugs with similar active ingredients, there is no significant difference between the two.
5 The Cytochrome P450 is the system of hemoproteins that are membrane-bound, and their primary function is detoxifying cellular metabolisms, xenobiotics, and homeostasis.
6 Poor metabolizers have double copies of no activity genes or low activity genes. This situation results in slow medication breakdowns, thus such antiplatelet medications as Clopidogrel fail to work as expected.
7 Drug administration largely depends on the time it will take for the drug to clear the person’s system to prevent withdrawal symptoms that may unpleasantly affect the individual upon quitting and avoid the excessive presence of chemical ingredients in the body.
8 Understanding a drug’s half-life helps determine the time it takes a drug’s concentration to stay consistent within the body, especially when administered regularly. The primary idea behind this explanation is that half-lives help understand the excretion rates of the drug.
9 Inhalation, oral, and parenteral drug actions are administering drugs through the airways, by way of mouth, and injection passing the skin, respectively. The choice of different drug actions determines the drug's duration to become prominent and effective in the body. Though it depends on particular drugs, their onset actions largely depend on drug action, for instance, most oral administrations take about twenty minutes.
10 The primary function of anticoagulants is suppressing collating factors synthesis within the blood.
Heparin produces anticoagulant effects by inactivating thrombin or binding with an antithrombin mechanism through a high-affinity pentasaccharide.
A low dose of subcutaneous heparin does not require aPTT monitoring because it is rarely associated with insignificant increases in bleeding, and thus, the mean normal value does not require monitoring the heparin therapy.
As an oral anticoagulant, warfarin inhibits the posttranslational alterations in coagulant factors dependent on vitamin K. this inhibition result in a gradual onset of the anticoagulation, which takes five to ten days. This period corresponds to the half-live soft factors; II, VII, IX, and X.
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