ID Beta-Lactams

Question 1

Penicillins MOA

Answer 1

Bind to PCN-binding proteins on bacterial cell wall/membrane; destroy cell wall by inhibiting transpeptidase (enzymes that cross-link peptidoglycan molecules to add strength) causing lysis (bacteriocidal)

Question 2

Penicillins AE

Answer 2

Allergic reaction, n/v/d

Question 3

Cephalosporins MOA

Answer 3

Bind to PCN-binding proteins on bacterial cell wall/membrane; destroy cell wall by inhibiting transpeptidase (enzymes that cross-link peptidoglycan molecules to add strength) causing lysis (bacteriocidal)

Question 4

Cephalosporin AE

Answer 4

Cross-reactivity to penicillin; pseudomembranous colitits; bone marrow suppression; nephrotoxicity

Question 5

Penicillins Prototype Drug

Answer 5

Penicillin G, Penicillin V

Question 6

Cephalosporins Prototype Drug

Answer 6

First-generation: cephalexin; second-generation: cefaclor, cefuroxime; third-generation: ceftazidime; fourth-generation: cefepime

Question 7

Carbapendems Prototype Drug

Answer 7

Imipenem (always combined with cilastatin to inhibit hydrolyzation by renal tubular dipeptidase)

Question 8

Carbapendems MOA

Answer 8

Bind to PCN-binding proteins on bacterial cell wall/membrane; destroy cell wall by inhibiting transpeptidase (enzymes that cross-link peptidoglycan molecules to add strength) causing lysis (bacteriocidal)

Question 9

Carbapendems AE

Answer 9

n/v, fever, imipenem may cause seizures

Question 10

Glycopeptides Prototype Drug

Answer 10

Vancomycin

Question 11

Glycopeptides MOA

Answer 11

Inhibit cell wall synthesis by attaching to the end of the peptidoglycan precursor units (D-alanyl-D-alanine terminus), thereby stopping peptidoglycan synthesis; bacteriocidal

Question 12

Glycopeptides AE

Answer 12

Flushing (red man syndrome), neutropenia; in rare cases: ototoxicity when combined with another ototoxic agent & nephrotoxicity

Question 13

Fluoroquinolones Prototype Drug

Answer 13

Ciprofloxacin

Question 14

Fluoroquinolones MOA

Answer 14

Inhibit DNA gyrase (aka topoisomerase II) in gram-neg organisms and topoisomerase IV in gram-pos organims; bacteriocidal

Question 15

Fluoroquinolones AE

Answer 15

Generally well-tolerated; n/v/d; tendon ruptures

Question 16

Aminoglycosides Prototype Drug

Answer 16

Gentamicin

Question 17

Aminoglycosides MOA

Answer 17

1. Inhibit protein synthesis by irreversibly binding the 30S ribosomal subunit; at low concentrations, they cause misreading of the mRNA by ribosomes; at high concentrations, they halt protein synthesis, trapping ribosomes at the AUG start codon 2. create fissures and pores in the outer cell membrane, resulting in leakage of intracellular contents and increased antibiotic uptake

Question 18

Aminoglycosides AE

Answer 18

Ototoxicity, nephrotoxicity (indicated by an increase in serum creatinine)

Question 19

Lincosamides Prototype Drug

Answer 19

Clindamycin

Question 20

Lincosamides MOA

Answer 20

Bind the 23S rRNA molecule of the 50S ribosome and inhibit peptidyl transferase, blocking the transfer of the new amino acid onto the growing chain; bacteriostatic; beneficial in toxin-producing infections

Question 21

Lincosamides AE

Answer 21

Pseudomembranous colitis (extremely high incidence of C. diff)

Question 22

Tetracyclines Prototype Drug

Answer 22

Tetracycline

Question 23

Tetracycline MOA

Answer 23

First enter microorganism, then bind reversibly to 16S sununit of the 30S ribosome and inhibits translation; bacteriostatic; Demecloclycline inhibits the binding of ADH to its receptor

Question 24

Tetracyclines AE

Answer 24

Significant n/v/d; mottling of teeth d/t Ca binding; photosensitivity; superinfection; diabetes insipidus; liver damage; kidney damage

Question 25

Macrolides Prototype Drug

Answer 25

Erythromycin

Question 26

Macrolides MOA

Answer 26

Bind to bacterial 50s ribosome and inhibit peptidyl transferase, blocking the transfer of the new amino acid onto the growing chain. Inhibition of protein synthesis does not typically kill bacteria cells, so these agents are generally bacteriostatic , but in high concentrations they can be bactericidal.

Question 27

Macrolides AE

Answer 27

Significant GI upset due to increased gut motility; Acute cholestatic hepatitis . Are better tolerated but can also cause liver impairment

Question 28

Oxazolidinones Prototype Drug

Answer 28

Linezolid

Question 29

Oxazolidinones MOA

Answer 29

blocks the translocation step of protein synthesis by binding the 23S rRNA of the 50S RSU. Therefore bacteriostatic. Can also result in human mitochondrial suppression (mitochondrial inhibitor) causing rare but serous side effects.

Question 30

Oxazolidinones AE

Answer 30

Rare but serious. Serotonin Syndrome, Hyperlactatemia and Metabolic Acidosis, Nerve Damage (neuropathies), and Hematologic (bone marrow suppression and low blood count)

Question 31

Sulfonamides Prototype Drug

Answer 31

Sulfamethoxazole

Question 32

Sulfonamides MOA

Answer 32

inhibitors of folate sythesis (bacteriostatic)

Question 33

Sulfonamides AE

Answer 33

Crystalluria, hematuria, nausea, vomiting, diarrhea, photosensitivity, hypersensitivity. Rare and Serious: Stevens-Johnson Syndrone (SJS), Blood Cell Problems (hemolytic Anemia, Aplastic Anemia, Thrombocytopenia), Kernicterus (jaundice in newborns)

Question 34

Metronidazole Prototype Drug

Answer 34

Metronidazole

Question 35

Metronidazole MOA

Answer 35

Prodrug: ferredoxin reduces nitrogen side chain from drug which results in production of toxic products that damage DNA. Effective for anaerobic bacteria

Question 36

Metronidazole AE

Answer 36

Nausea, Metallic Taste, CNS toxicity (ataxia, encephalopathy, siezure), RARE: neutropenia, pacreatitis, peripheral neuropathy, hepatitis

Question 37

Ethambutol Prototype Drug

Answer 37

Ethambutol (EMB or E)

Question 38

Ethambutol MOA

Answer 38

Disrupts formation of the tuberculous cell wall by blocking arabinosyl transferases. bacteriostatic , suppress the growth of TB but does not kill it

Question 39

Ethambutol AE

Answer 39

Neurologic, ( Optic neuritis, perminant blindness, red-green color blindness, peripheral neuropathy)Rash, and Fever

Question 40

Isoniazid Prototype Drug

Answer 40

Isoniazid (INH or H)

Question 41

Isoniazid MOA

Answer 41

Inhibits mycobacterial cell wall synthesis

Question 42

Isoniazid AE

Answer 42

Hepatitis, Peripheral Neuropathy, mild CNS effects, and Rash

Question 43

Pyrazinamide Prototype Drug

Answer 43

Pyrazinamide (PZA or Z)

Question 44

Pyrazinamide MOA

Answer 44

Prodrug: first needs to be converted to pyrazinoic acid by a mycobacterial enzyme called pyrazinamidase. This inhibits cell wall synthesis by inhibiting enzyme called fatty acid sythase I .Drug is active only if the bacterium is in an acidic environment

Question 45

Pyrazinamide AE

Answer 45

Serous: Hepatic Injury (drug induced hepatitis) More Common: Arthalgia (joint pain), Increased uric acid, Anorexia, Nausea and Vomiting

Question 46

Rifamycins Prototype Drug

Answer 46

Rifampin (rifampicin)

Question 47

Rifamycins MOA

Answer 47

Inhibit bacterial RNA sythesis by binding prokaryotic (bacterial) RNA polymerase. bactericidal for extracellular and intracellular bacteria. is highly lipophilic

Question 48

Rifamycins AE

Answer 48

Common: Discoloration of secretions (tears, urine, sweat, stool, saliva), Cholestatic Jaundice and Hepatitis, Rash Rare but Serous: Acute interstitial nephritis (AIN) and Thrombocytopenia

Question 49

CCR5 Antagonists Prototype Drug

Answer 49

Maraviroc

Question 50

CCR5 Antagonists MOA

Answer 50

Block interaction of gp120 (HIV envelope glycoprotein on cell surface-eventually binds w/ CCR5 to initiate conformational change) w/ CCR5 (chemokine coreceptor), preventing viral entry into human cells; Patients w/ HIV may express CXCR4 or CCR5 or a combo of both ("dual-mixed"); CCR% antagonists typically used for those w/ CCR5; use of CCR5 antagonists in patients who are dual-mixed leads to selection of CCRX4 & resistance

Question 51

CCR5 Antagonists AE

Answer 51

Antiretrovirals typically administered in combo regimens therefore tough to decipher side effects; However, postural hypotension & syncope is common; Hepatotoxicity (rare); Cardiovascular events such as MI

Question 52

Fusion Inhibitors Prototype Drug

Answer 52

Enfuvirtide

Question 53

Fusion Inhibitors MOA

Answer 53

Mimics the HIV machinery required to fuse to the CD4 cell; Competes with the HIV proteins & prevents entry of the virus into the CD4 cell; gp120 binds HIV & activates gp41-->gp41 changes conformation & creates pore into cell-->enfuvirtide binds gp41 & prevents conformational change

Question 54

Fusion Inhibitors AE

Answer 54

Injection site irritation; Peripheral neuropathy

Question 55

Integrase Inhibitors Prototype Drug

Answer 55

Raltegravir

Question 56

Integrase Inhibitors MOA

Answer 56

Responsible for incorporating viral DNA into the host genome; Prevent the formation of covalent bonds w/ host DNA therefore preventing incorporation of HIV into host genome

Question 57

Integrase Inhibitors AE

Answer 57

Well-tolerated

Question 58

Nucleoside Reverse Transcriptase Inhibitors Prototype Drug

Answer 58

Zidovudine

Question 59

Nucleoside Reverse Transcriptase Inhibitors MOA

Answer 59

An enzyme that transcribes viral RNA into viral DNA; Upon entry into the cell are converted to nucleotides by host cell kinases; The nucleotides then compete w/ endogenous nucleosides for incorporation into viral DNA; act as competitive inhibitors of reverse transcriptase; Once incorporated into DNA, cause termination of DNA chain (halts viral replication); also inhibit host cell DNA polymerase; not specific for HIV-1 however nonnucleoside may act directly against HIV-1

Question 60

Nucleoside Reverse Transcriptase Inhibitors AE

Answer 60

Myalgia; Headache; Diarrhea; Lactic acidosis; Lipodystrophy; Peripheral neuropathy; Pancreatitis; Hepatotoxicity; Bone marrow suppression; Hypersensitivity; Acute renal failure; Stomatitis & oral ulcers

Question 61

Nonnucleoside Reverse Transcriptase Inhibitors Prototype Drug

Answer 61

Nevirapine

Question 62

Nonnucleoside Reverse Transcriptase Inhibitors MOA

Answer 62

bind to a site distant from the active site of the reverse transcriptase and induce a conformational change in the enzyme; NO ACTIVITY against DNA polymerase; Binding is very specific to reverse transcriptase

Question 63

Nonnucleoside Reverse Transcriptase Inhibitor AE

Answer 63

Rash (macular or papular- pruritic); Rash may progress to Stevens-Johnson syndrome; Hepaptitis (more common in females during pregnancy, result of hypersensitivy reaction);

Question 64

Protease Inhibitors Prototype Drug

Answer 64

Saquinavir

Question 65

Protease Inhibitors MOA

Answer 65

Disrupts viral maturation; Bind to proteases and prevent viral maturation which produces immature, noninfectious virus particles

Question 66

Protease Inhibitors AE

Answer 66

GI (n/v/d); Hyperlipidemia; Lipodystrophy (fat redistribution); Hyperglycemia/insulin resistance (inhibit activity of glucose transporter GLUT-4); Crystalluria/nephrolithiasis; Hyperbilirubinemia

Question 67

Uncoating Inhibitors Prototype Drug

Answer 67

Amantadine

Question 68

Uncoating Inhibitors MOA

Answer 68

Prevents the virus from uncoating not allowing the viral DNA to be translated into mRNA; Uncoating is mediated by a M2 protein which serves as a proton channel facilitating the dissociation of the RNA-protein complex; This dissociation is pH-dependent so when drug prevents the influx of protons through M2, prevent dissociation from occuring; may also inhibit a late step of viral assembly

Question 69

Uncoating Inhibitors AE

Answer 69

CNS-Amantadine (nervousness, lightheadedness, difficulty concentrating, insomnia); Loss of appetite, Nausea

Question 70

Neuroaminidase Inhibitors Prototype Drug

Answer 70

Zanamivir

Question 71

Neuraminidase Inhibitors MOA

Answer 71

Influenza viruses possess 2 surface glycoproteins. Changes in these result in new diseases year after year; cleave the sialic acid residues that are bound to viral hemagglutinin & result in the release of new virus from cells; block the cleavage of sialic acid residues & prevent the release of new virus from early infected cells (earlier administration of drug is more successful)

Question 72

Neuraminidase Inhibitors AE

Answer 72

Bronchospasms may occur/worsening of respiratory symptoms; GI symptoms (n/v/abd cramping)

Question 73

Nucleoside Analogues Prototype Drug

Answer 73

Acyclovir

Question 74

Nucleoside Analogues MOA

Answer 74

Act as DNA polymerase inhibitors; Reduces DNA synthesis & viral replication; Serve as guanosine analogs; Important step in viral life cycle = synthesis of viral DNA; Viral & host cell kinases convert the nucleoside analogues to active nucleoside triphosphates; Nucleoside triphosphates compete w/ viral DNA polymerase for part of the primer strand of viral DNA; Some nucleoside analogues (acyclovir & valacyclovir) cause chain termination when incorporated into DNA strand; Penciclovir inhibits DNA elongation; Selective toxicity based upon (1) affinity for HSV thymidine kinase 200x greater for viral enzyme than human enzyme & (2) greater affinity for viral vs. human DNA polymerase

Question 75

Nucleoside Analogues AE

Answer 75

Nausea & diarrhea, Rash, Headache, CNS (confusion, hallucinations, tremor) - Acyclovir & valacyclovir - Esp. renal patients; Nephrotoxicity - Acyclovir & valacyclovir; UNIQUE Hematologic (leukopenia, thrombocytopenia); Reproductive (aspermatogenesis)