PHARM STUDY GUIDE QUIZ 1 WITH-ANSWERS OB WITH EXPLAINED ANSWERS 100% CORRECT DOWNLOAD TO S, Exams of Nursing

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MODULE 1

1) Discuss the significance of the Cytochrome P450 system on metabolism of drugs.

1. It is a group of 12 closely related enzyme families. CYP1, CYP2, CYP metabolize drugs. The other 9 families metabolize endogenous compounds (ex. Fatty acids, steroids). **2) Discuss the major hepatotoxic drugs and possible effects on drug metabolism. 1.

3. List various routes of drug elimination—review normal renal function including glomerular filtration, passive tubular reabsorption and active tubular secretion; describe the implications on drug clearance and how elimination affects prescribing.

4. Discuss terms used to describe drug actions-agonist, partial agonist, antagonist. 1.** Agonist: molecules that activate receptors 2. Partial agonist: Only has moderate intrinsic activity. Maximal effect that a partial agonist can produce is lower than that of a full agonist. 3. Antagonist: Produce their effects by preventing receptor activation by endogenous regulatory molecules and drugs. 5) Discuss the impact of food on drug absorption, drug metabolism and on drug toxicity and action—as well as the timing of drug administration. LIFESPAN 1. Hepatic metabolism and GFR increase during pregnancy, dosages of some drugs may need to be increased. 2. Rate of albumin to water decreases 1. Third trimester: Renal blood flow is doubled and renal excretion is accelerated (drugs excreted rapidly) 2. Tone and mobility of bowel decrease 3. Prolongation of drug effects Total (½ life increases)

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3. Understand stages of development in pregnancy 1. Conception: through week 2 2. Embryonic period: week 3-week 8 a) Gross malformations can be produced by teratogens 3. Fetal period: week 9-delivery 4. Understand pregnancy labeling 1. 3 categories now a) Pregnancy, lactation, male & female reproductive potential 5. How do you decrease risk in the infant during breastfeeding? 1. Take meds immediately after breastfeeding, avoid drugs that have long half-lives, choose drugs that tend to be excluded from milk, avoid drugs that are known to be hazardous. 6. How do pediatric patients differ in their response to medications? 1. Absorption a) Oral? 1. Neonates: drug remain in the stomach longer which increases the levels, low acidity can affect the absorption of acid labile drugs b) Parenteral? 1. Reponses are slow and erratic. 2. Infancy: absorption is more rapid than in neonates & adults 3. Best avoided in infants c) Transdermal? 1. Greater skin permeability which increases topical drug absorption and increases the risk for toxicity 2. Distribution a) Protein binding 1. Neonates: less protein-binding—increased availability of

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highly protein bound drugs such as phenytoin, diazepam, and phenobarbital. Reduced dosages needed in these highly bound drugs. b) Blood Brain Barrier

1. Not fully developed at birth, drugs have easy access to the CNS, doses should be reduced. 3. Metabolism a) Hepatic function? 1. Liver hasn’t reached full maturation—sensitive to drugs eliminated by the CYP450. Liver’s ability to metabolize drugs increases about one month after birth. b) T half life 1. Decreased by as much as 48-72 hours 4. Excretion a) Renal? 1. GFR is significantly reduced at birth, drugs eliminated by the kidneys must be given in a reduced dosage and longer dosing intervals. 2. What are the BON rules and regulations for prescriptive authority for the advance practice nurse? 1) Texas is very restricted **2) Describe the pharmacokinetic processes of absorption, distribution, metabolism and elimination and how differences in these areas affect drug action.

1. Absorption 1.** Drug’s movement from the site of administration into the blood. 2. Distribution 1. Drug’s movement from the blood into the interstitial space of tissues and from there into cells.

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3. Metabolism 1. Biotransformation is the enzymatically mediated alteration of drug structure. 4. Elimination 1. Combination of metabolism and excretion 3) Compare and contrast pharmacokinetics and pharmacodynamics of special populations—pediatrics, older adults and those that are pregnant. 1. Pediatrics—they have organ immaturity, elderly—they have organ degeneration, loss of nephrons, excretion of drug is decreased and you have to give this population a lower dose of medication. Medication can pass through milk of lactating females. 4) Analyze a drug interaction to determine an appropriate course of action. 1. Basic mechanism of drug-drug interactions through pharmacokinetic interactions are altered absorption, altered distribution, altered metabolism, and altered renal excretion. **5) Identify medications with a narrow therapeutic index requiring drug level monitoring.

6. Discuss the effect of ionization and pH on absorption. 1.** Drugs that are weak acids are best absorbed in acidic environments. Acidic drugs accumulate on the alkaline side, basic drugs accumulate on the acidic side known as ion trapping. Ionization of the drugs is pH dependent, when the pH and the fluid on one side of the membrane differs from the pH on the other side, drug molecules tend to accumulate on the side where the pH most favors ionization. 7) Discuss factors affecting drug distribution. 1. Competition for protein binding and alteration of extracellular pH 8) Discuss barriers affecting drug distribution—such as placental membrane, blood brain barrier and volume of distribution.

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1. Placental membrane: drugs are easily passed through the placental membrance 2. Blood brain barrier: the PGP pumps drugs back into the blood and thereby limits their access to the brain. 3. Volume of distribution: 9) Discuss the “first-pass effect”—what effect can this have on distribution of a drug? 1. Rapid hepatic inactivation of certain oral drugs. When drugs are absorbed by the GI tract, they are carried directly to the liver through the hepatic portal vein

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before entering the systemic circulation. If the capacity of the liver to metabolize the drug is extremely high, this drug can be completely inactivated on its first pass through the liver.

1. What education needs to be given to parents? 1. What to do if child spits out medication or throws it up 2. Effective education: dosage size and timing, route, technique of administration, duration of treatment, how to store the drug, nature and time course of the desired response, nature and time course of adverse reactions. 2. How do you convert pounds to KG? 1. Divide weight by 2. 3. What is definition of polypharmacy? Is polypharmacy always inappropriate? What is Beer’s List? 1. Polypharmacy: 3 or more prescription drugs in conjunction-+ with 3 or more dietary supplements. 2. No 3. List that identifies drugs with a high likelihood of causing adverse effects in the elderly

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4. What are pharmacodynamic and pharmacokinetic differences in geri patients? 1. Absorption? a) GI 1. Produce less acid and fewer parietal cells 2. Bioavailability decreased 3. Rate of absorption decreased 2. Distribution? a) Lean Body Mass 1. Drugs accumulate in adipose tissues because lean muscle mass decreases by 20% b) Body Water 1. Decrease by 10-15%-drugs reach higher serum concentrations c) Albumin 1. Lowered—leads to higher levels of free or unbound drugs 3. Metabolism? a) Hepatic 1. Decreased with age—decreases drug clearance b) T half life 1. Increases—alters drug-drug interactions 4. Excretion? a) Renal 1. Decreases—which decreases renal clearance of drugs ANTIMICROBIALS

1. Differentiate Bacteriostatic and Bactericidal.
2. Bacteriostatic: can slow bacteria growth and do NOT cause cell death ■ Bacteriostatic: ECSTaTiC ■ E rythromycin ■ C lindamycin ■ S ulfamethoxazole ■ T rimethoprim ■ a ■ T etracycline ■ i ■ C hloramphenicol ■ Bacterialcidal: Very Finely Proficient At Cell Murder ■ V ancomycin ■ F luoroquinolones ■ P enicillin ■ A minoglycosides ■ C ephalosporins ■ M etronidazole

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2. Baterialcidal: directly lethal to the bacteria
3. What is the difference between broad spectrum and narrow spectrum?
4. Broad spectrum: active against a wide variety of microbes.
5. Narrow spectrum: only active against a few species of bacteria or micro-organisms
6. Which is preferred?
7. Narrow spectrum
8. What are antibiotic classifications?
9. Classifications by susceptible organisms
10. Classified by mechanism of action
11. What is empiric antibiotic use? Therapeutic use?
12. Initiate treatment before you know what the results of the test-- Treat with broad-spectrum antibiotic for initial treatment and once you get culture and drug sensitivity then you can use narrow spectrum antibiotic.
13. Which antibiotics work by weakening the cell wall?
14. Penicillins

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7. Beta Lactam?
   1. Penicillins (penicillin G, Ampicillin, amoxicillin, pipercillin)
   2. Carbapenems (ztreonam, Imipenem, Meropenem, Ertapenem)
   3. Cephalosporins (Cefazolin, ceftriaxone, cefotetan)
   4. Vancomycin
   5. Lypoglycoproteins (telavancin)
   6. Monobactrams (aztreonam)
   7. Fosfomycin
8. What are the medications that react with PCN? 1. Aminoglycosides, bacteriostatic agents, and probenecid
9. What organisms are susceptible to PCN? 1. Gram-positive bacteria and gram-negative
10. Beta lactams 1. Penicillins, cephalosporins and carbapenems (drugs that end in -nem and -nam) b) Mechanism of action: weaken cell wall and promote bacterial lysis and death. Active only against bacteria that is undergoing growth and cell division. c) allergy potential between penicillin and cephalosporins* d) Allergic Reaction 1. Immediate: 2-30 minutes after dose 2. Accelerated: 1-72 hours after dose 3. Delayed: days to weeks 4. Treatment: epinephrine (IM or SubQ or IV), respiratory support. e) Drug-drug interactions: aminoglycosides, bacteriostatic agents, probenecid f) Penicillin G AKA Penicillin Mediated by IgE antibodies

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1. Bactericidal to gram-positive and gram-negative bacteria. 2. Drug of choice g) Ampicillin and Amoxicillin 1. Broad spectrum 2. Gram-negative bacilli i. Haemophilus influenza ii. E. Coli iii. Salmonella iv. Shigella 3. Adverse reaction i. Rash ii. Diarrhea h) Piperacillin 1. Extended-spectrum penicillin 2. Fights against: pseudomonas, enterbacter, proteus, bacteroides fragilis, klebsiella 3. Administered: parenterally via IV

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4. Adverse reaction: bleeding secondary to disrupting platelet aggregation. i) Penicillin combination (beta-lactamase inhibitors) 1. Ampicillin/sulbactam 2. Amoxicillin/clavulanate 3. Piperacillin/tazobactam j) Resistance issues with penicillin 1. Primarily against Staphylococcus aureus i. MRSA (sensitive) 2. Developed to resist penicillinase 3. Hepatotoxicity 4. Dose reduction in renal insufficiency k) Nephrotoxicity* 1. Kidney toxicity 2. Monitor renal function 2. Generations of cephalosporins a) Mechanism of action: bind to penicillin-binding proteins and disrupt cell wall synthesis, activate autolysis, damage cell wall. b) Most affective in cells undergoing active growth and division. c) Drug-drug interaction: probenecid d) Cefazolin & Ceftriaxone -do not give with alcohol e) Cefotetan & Ceftriaxone (decreases vitamin K metabolism)-do not give with warfarin f) Ceftriaxone -do not give with calcium g) Adverse effects: allergic reaction, bleeding, thrombophlebitis

1. 1 st:

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2. 2 nd
3. 3 rd i. Destroyed by beta-lactamases ii. No CSF iii. Gram + iv. Narrow spectrum v. Used for prophylaxis, surgical prophylaxis vi. Rarely used for active infections i. Less sensitive to destruction ii. No CSF iii. Less gram + more gram – iv. Rarely used for active infections v. Effective against H. Influenza, klebsiella, pneumococci, and staphylococci vi. Good for upper respiratory infections, otitis media, bacterial sinusitis i. Highly resistant ii. Enters CSF* (good treatment for meningitis) iii. Highly active against gram - iv. Preferred for severe infections

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4. 4 th
5. 5 th i. Highly resistant ii. Enters CSF iii. Excellent gram – coverage iv. Commonly used to treat healthcare & hospital associated pneumonia (especially caused from pseudomonas) i. Used for infections associated with MRSA h) Thrombophlebitis with cephalosporins
6. Give by slow IV piggyback
7. Dilute drug (50-100 mL IV solution)
8. Carbapenems ( Imipenem, meropenem, ertapenem, doripenem ) a) Very broad antimicrobial spectrum b) Not effective against MRSA c) Imipenem
9. Good for treating mixed infections ii. staph aureus iii. gram – bacilli
10. binds to PBP1 and PBP d) Adverse effects
11. GI: nausea and vomiting
12. Skin rash and pruritus
13. Fever e) Drug-drug interaction: valproate (break through seizures can occur) f) Administered only parenterally 4. Vancomycin

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g) No beta-lactam ring h) Uses and coverage

1. MRSA and C diff infections (IV)*
2. Oral is only used for c. diff (PO)*
3. Penicillin allergic patients for streptococcal endocarditis (rotten teeth that give a patient heart problems) i) Adverse Effects**
4. Thrombophlebitis
5. Thrombocytopenia
6. Red man syndrome* i. Hypotension ii. Histamine flush iii. Not an allergic reaction* j) Nephrotoxicity and ototoxicity*
7. Monitor renal function
8. Lypoglycoproteins k) Telavancin
9. Uses

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i. Gram + bacteria ii. Only given IV iii. ONLY used in vancomycin-resistant infections

2. Adverse Effects i. Taste disturbance ii. Nausea iii. Vomiting iv. Foamy urine v. Red man syndrome vi. Prolong QT interval vii. BLACK BOX WARNING: mortality increases in pts. With hospital-acquired or ventilator- associated pneumonia and creatinine clearance <50.
3. Drug-drug interactions: NSAIDS or ACE Inhibitors (damage kidneys), Clarithromycin, ketoconazole (cause prolonged QT interval)
4. Monobactrams l) Aztreonam
5. Binds to PBP
6. Narrow spectrum
7. Active against gram – bacteria i. Neisseria species ii. H. Influenza iii. Pseudomonas iv. Klebsiella v. Proteus vi. Serratia

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vii. Salmonella viii. Shigella

4. Highly resistant to beta lactamases 7. Fosfomycin a) Single dose therapy b) UTI caused by E. Coli or enterococcus faecalis c) Mechanism of action
5. Kills bacteria by partially preventing cross-linking of peptidoglycan strands d) Adverse effects
6. Diarrhea
7. Headache
8. Vaginitis
9. Nausea
10. Abdominal pain
11. Rhinitis
12. Drowsiness
13. Dizziness e) Take with or without food

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f) Symptoms improve within 2-3 days after taking BACTERIOSTATIC INHIBITORS (suppress growth, do not kill)

1. Tetracyclines ( tetracycline, demeclocycline, doxycycline, minocycline ) a) Broad spectrum b) Work against gram + and – c) Mostly used outpatient d) Extensive use = increased in bacterial resistance e) Uses 1. Chylamydial infections and other STDs 2. Helicobacter pylori (causes ulcers in the duodenal and gastric) 3. Acne 4. Skin infections 5. Anthrax (doxycycline) 6. Infectious disease 7. PUD 8. Periodontal disease 9. RA 10. RMSF 11. Pneumonia 12. Lyme disease f) Why can’t we give to children under 8 and pregnant women?* 1. Can irreversibly stain teeth (4 months-8 years old)* 2. Impact skeletal development in babies* g) Photosensitivity* 3. Wear sunscreen

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h) Adverse effects

1. Nausea, cramps, epigastric burning
2. Create superinfections—c. diff
3. Hepatotoxicity—IV form i) tetracycline with iron, vitamins, or calcium – bioavailability*
4. Impaired absorption of antibiotic
5. If you want to take iron, vitamins, or calcium leave 2 hours in between tetracyclines 2. Macrolides a) Broad spectrum b) Erythromycin
6. High dose IV is cidal
7. Low dose PO is static
8. Food increases absorption
9. Metabolized by CYP3A4 system
10. Drug-drug interactions: theophylline, carbamazepine, warfarin, verapamil, diltiazem, HIV protease inhibitors, simvastatin cipro

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6. Uses i. Alternative to PCN in allergic patients ii. Atypical infections
7. Group A strep
8. Corynebacterium diphtheriae
9. Whooping cough
10. Chlamydia and Mycoplasma (walking pneumonia)
11. Side effects i. GI difficulties most common with oral erythromycin 1. N/V/D, abdominal cramping, hepatotoxicity ii. Less side effects with newer macrolides c) Azithromycin
12. Cause QT prolongations** d) Clindamycin (Cleocin)
13. Bacteriostatic
14. BLACK BOX WARNING: Promote severe c. diff in elderly patients
15. Uses i. Anaerobic bacteria, gram – and +
16. Used as alternate to penicillin
17. Adverse effects i. Hepatic toxicity ii. Blood dyscrasias iii. Diarrhea iv. Hypersensitivity reactions

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3. Oxazolidiones ( Zyvox or Linezolid ) a) Used to treat VRE and MRSA b) Very expensive c) Limited use due to resistance d) Gram + bacteria, NO gram - bacteria 1. Enterococcus 2. MRSA 3. Staphylococcus epidermidis 4. Strep pneumonia e) Adverse effects 1. Diarrhea 2. Nausea 3. Vomiting 4. Headache 5. Myelosuppression f) Drug-drug interactions 1. MAOIs and Tedizolid 4. Ketolides

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a) Telithromycin

1. Uses i. Strep pneumonia
2. Adverse effects i. Severe liver damage ii. GI effects iii. Visual disturbances iv. Prolonged QT interval v. BLACK BOX WARNING: muscle weakness and shouldn’t be used in myasthenia gravis due to respiratory failure. 5. Streptogramins a) Dalfopristin
3. Uses i. Vancomycin-resistant enterococcus
4. Adverse effects i. Hepatic toxicity
5. Drug-drug interactions: CYP3A4 system b) Chloramphenicol
6. Uses i. Life threatening infections
7. Adverse effects i. Reversible bone marrow depression ii. Fatal aplastic anemia (BLACK BOX WARNING) iii. Gray syndrome iv. GI effects v. Peripheral neuropathy 6. Tigecycline

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a) Broad spectrum bacteria b) Causes increased mortality (not used unless other infection isn’t responding to other agents)

7. Retapamulin and mupirocin a) Topical used for impetigo 8. Mupirocin a) Used in nostrils for MRSA for people who are carriers 9. Aminoglycosides ( gentamycin, tobramycin, amikacin ) a) Uses and coverage 1. Gram negative only i. Serious or life-threatening infections*

1. Alone or with other antibiotics ii. Local treatment (ear/eye infection) 2. Bactericidal 3. Narrow spectrum b) Sensitive organisms**

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1. E. coli, Klebseilla pneumoniae, serratia marcescens, proteus mirabilis, pseudomonas aeruginosa c) Peaks and troughs**
2. Daily dosing i. Peak levels need to be drawn 30 minutes after IM injection or IV infusion ii. Trough levels need to be drawn one hour before next dose—value should be close to zero
3. Divide dosing iii. Trough levels need to be drawn just before the next dose
4. Peak iv. Measures the adequacy of dose (needs to be high enough to kill bacteria)
5. Trough v. If elevated=toxicity (love enough to minimize toxicity) d) Adverse effects**
6. Nephrotoxicity and ototoxicity*
7. Hypersensitivity reactions
8. Blood dyscrasias e) Drug-drug interactions
9. Neuromuscular blocking agents
10. General anesthetics
11. Cephalosporins, polymyxins, vancomycin, cyclosporine, aspirin (toxic to kidneys when used in combination) f) Beneficial drug-drug interactions
12. Penicillin

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2. Cephalosporins
3. Vancomycin g) Do not give to pt. with myasthenia gravis
4. Reversal treatment of choice is calcium salt h) Gentamycin
5. Uses vi. Gram – bacilli
6. Pseudomonas, e. coli, klebsiella, Serratia, proteus mirabilis
7. Used where resistance is high in hospitals
8. Adverse effects vii. Nephrotoxicity, ototoxicity 10. Sulfonamides a) Broad spectrum b) Mechanism of action**
9. Suppress bacterial growth by inhibiting tetrahydrofolic acid (derivative of folic acid or folate) c) Uses

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1. UTIs (main use)
2. Gram negative
3. Others i. Nocardiosis ii. Malaria iii. Ulcerative colitis iv. Toxoplasmosis v. Chlamydia d) Adverse effects
4. Skin, skin, skin i. Skin rashes & itching ii. Stevens-Johnson syndrome iii. Photosensitivity
5. Hematologic effects i. Hemolytic anemia ii. Kernicterus
6. Renal damage e) Drug-drug interactions**
7. Phenytoin, glipizide, glyburide (inhibit hepatic metabolism)
8. Thiazide (Celebrex) diuretics and sulfides (cross- hypersensitivity) f) Resistance to sulfonamides
9. Gonococci, meningococci, streptococci, shigellae g) Topical sulfonamides ( silver sulfadiazine and mafenide )
10. Used to suppress colonization in pt. with 2 nd^ and 3 rd^ degree burns
11. Mafenide application painful i. Can cause acidosis