Pharmacology Exam 3

Front 1

Which cells have a THICK proteoglycan layer?

A. Gram +
B. Gram –

Back 1

A. Gram +

Front 2

Which cells have a THIN proteoglycan layer?

A. Gram +
B. Gram –

Back 2

B. Gram –

Front 3

N-acetylmuramic acid (NAMA), N-acetylglucosamine (NAG), and Penta peptide Glycine make up which part of a bacterial cell wall?

A. LPS
B. Plasma membrane
C. Peptidoglycan
D. Periplasmic space

Back 3

C. peptidoglycan

Front 4

What happens in the 1st stage of peptidoglycan formation?

A. cross-linking NAMA-NAMA by transpeptidase
B. D-alanine added to NAMA-UDP
C. Binding of P-C55 onto NAMA to form long polymer

Back 4

B. D-alanine added to NAMA-UDP

Front 5

What happens in the 2nd stage of peptidoglycan formation?

A. cross-linking NAMA-NAMA by transpeptidase
B. D-alanine added to NAMA-UDP
C. Binding of P-C55 onto NAMA to form long polymer

Back 5

C. Binding of P-C55 onto NAMA to form long polymer

Front 6

What happens in the 3rd stage of peptidoglycan formation?

A. cross-linking NAMA-NAMA by transpeptidase
B. D-alanine added to NAMA-UDP
C. Binding of P-C55 onto NAMA to form long polymer

Back 6

A. cross-linking NAMA-NAMA by transpeptidase

Front 7

Match the following events of peptidoglycan formation to their site of action:
- cross-linking NAMA-NAMA by transpeptidase
- D-alanine added to NAMA-UDP
- Binding of P-C55 onto NAMA to form long polymer

A. cytoplasm
B. cell membrane
C. cell wall

Back 7

A. CYTOPLASM = D-alanine added to NAMA-UDP

B. CELL MEMBRANE = Binding of P-C55 onto NAMA to form long polymer

C. CELL WALL = cross-linking NAMA-NAMA by transpeptidase

Front 8

Which of the following enzymes attack the β-lactam ring of penicillin?
(select all)

A. amidase
B. penicillinase
C. β-lactamase

Back 8

B. penicillinase
C. β-lactamase

Front 9

Which of the following enzymes attack the R group of penicillin?
(select all)

A. amidase
B. penicillinase
C. β-lactamase

Back 9

A. amidase

Front 10

The ______ domain of PBP (penicillin binding protein) forms linear glycan strands (connects NAMA to NAG)

A. Transglycolase (TG)
B. Transpeptidase (TP)
C. serine residue

Back 10

A. Transglycolase (TG)

Front 11

The ______ domain of PBP (penicillin binding protein) cross-links the peptide subunits (connects NAMA to NAMA)

A. Transglycolase (TG)
B. Transpeptidase (TP)
C. serine residue

Back 11

B. Transpeptidase (TP)

Front 12

The ______ domain of PBP (penicillin binding protein) is required for covalent bond formation & is conserved in all members of the PBP family

A. Transglycolase (TG)
B. Transpeptidase (TP)
C. serine residue

Back 12

C. serine residue

Front 13

T/F
All β-lactam antibiotics that bind Penicillin Binding Proteins (PBPs) belong to acyl serine transferases

Back 13

True

Front 14

How can elaboration of PBPs lead to Penicillin resistance?

Back 14

Causes ↓ affinity for β-lactams

(if penicillin can't bind PBPs → no cell death)

Front 15

Name all the ways Bacteria can become penicillin resistant

A. Elaboration of normal PBPs
B. Inability of drug to penetrate
C. Efflux pumps
D. Production of β-lactamase

Back 15

A. Elaboration of normal PBPs
B. Inability of drug to penetrate (LPS, no porins, etc.)
C. Efflux pumps
D. Production of β-lactamase

Front 16

_____ cells secrete β-lactamase extracellularly in large amounts

A. Gram +
B. Gram –

Back 16

A. Gram +

Front 17

In _____ cells β-lactamase is located in the periplasmic space in small amounts.

A. Gram +
B. Gram –

Back 17

B. Gram –

Front 18

T/F
Penicillins penetrate phagocytic cells

Back 18

False

(don't penetrate phagocytic cells)

Front 19

T/F
Penicillin G is superior to Penicillin V because it is acid stable and more readily absorbed.

Back 19

False

(Pen V is superior to Pen G)

Front 20

Which is used to treat cellulitis, bacterial endocarditis, Streptococcal infections, and some STDs?

A. Penicillin G
B. Penicillin V

Back 20

A. Penicillin G

Front 21

Which is used to treat tonsilitis, pharyngitis, skin infections, and odontognic infections?

A. Penicillin G
B. Penicillin V

Back 21

B. Penicillin V

Front 22

Which drug would you use for Staph. aureus (contain β-lactamase)

A. Penicillin V
B. Amoxicillin
C. oxacillin
D. carbenicillin

Back 22

C. oxacillin

(β-lactamase resistant)

Front 23

T/F
Ampicillin is superior to amoxicillin because it is acid stable and more readily absorbed

Back 23

False

(Amoxicillin is superior to Ampicillin)

Front 24

Which of the following drugs are β-lactamase resistant?
(select all)

A. naficillin
B. ampicillin
C. oxacillin
D. cloxacillin
E. amoxacillin
F. carbenicillin
G. dicloxacillin

Back 24

A. naficillin
C. oxacillin
D. cloxacillin
G. dicloxacillin

Front 25

_____ extends the spectrum of ampicillin to include most strains of P. aeruginosa

A. carbecillin
B. ticarcillin
C. piperacillin

Back 25

C. piperacillin

Front 26

What is the most common side effect of penicillins?

Back 26

Hypersensitiity

Front 27

T/F
Allergy to one penicillin poses a greater risk to other penicillins

Back 27

True

Front 28

T/F
Penicillin only causes an allergic response when bound to a protein

Back 28

True

(Penicillin is a hapten)

Front 29

What is a major adverse side effect of β-lactamase resistant penicillins?

A. ↓ platelet aggregation
B. neutropenia
C. hypernatremia & hypokalemia

Back 29

B. neutopenia

Front 30

What is the major adverse side effect of taking any penicillin-based antibiotic?

Back 30

pseudomembranous colitis

Front 31

Penicillins should NEVER be administered at the same time as:

A. macrolides
B. aminoglycosides
C. anti-histamines
D. anticoagulants

Back 31

B. aminoglycosides

(stagger by 1-2 hrs)
(Carboxy- or ureidopenicillins & aminoglycosides are synergistic in their anti-pseudomonas activity)

Front 32

In cephalosporins, ___ decides the antibacterial activity, resistance to β-lactamase, and stability in acid

A. R1
B. R2

Back 32

A. R1

Front 33

In cephalosporins, ___ effects metabolism and pharmokinetics

A. R1
B. R2

Back 33

B. R2

Front 34

Describe how penicillins inhibit bacterial growth

Back 34

Bind and acylate transpeptidase domain of PBP (of bacteria)
↓
acylation inhibits PBPs
(prevents cross-linking of peptidoglycan)
↓
Structural irregularities in cell wall
↓
Cell lysis

(similar to cephalosporins)

Front 35

How do cephalosporins inhibit bacterial growth?

Back 35

Acylate & inhibit PBPs
↓
Inhibits cross-linking of peptidoglycan (transpeptidase)
↓
structural irregularities
↓
Cell lysis

(similar to penicillin)

Front 36

Rank the cephalosporin generation for activity against Gram + bacteria

- 1st generation
- 3rd generation

Back 36

1st > 3rd

Front 37

Rank the cephalosporin generation for activity against Gram – bacteria

- 1st generation
- 2nd generation
- 3rd generation

Back 37

3rd > 2nd > 1st

Front 38

Have an extended spectrum of activity than 3rd generation cephalosporins.

A. 1st generation
B. 2nd generation
C. 4th generation
D. 5th generation

Back 38

C. 4th generation cephalosporin

Front 39

Cephalosporins which contain drugs that are active against pseudomonas

A. 1st generation
B. 2nd generation
C. 3rd generation
D. 4th generation
E. 5th generation

Back 39

C. 3rd generation cephalosporin

Front 40

Cephalosporins that are active against MRSA, penicillin-ristant Strep. pneumonia, and P. arugenosa

A. 1st generation
B. 2nd generation
C. 3rd generation
D. 4th generation
E. 5th generation

Back 40

E. 5th generation

Front 41

Cephalosporin least susceptible to β-lactamase

A. 1st generation
B. 2nd generation
C. 3rd generation
D. 4th generation
E. 5th generation

Back 41

D. 4th generation

Front 42

T/F
Cephalothin is more susceptible to β-lactamase than cefazolin

Back 42

False

(cefazolin is more susceptible than cephalothin)

Front 43

T/F
Both penicillins and cephalosporins can penetrate CSF and cross the placenta

Back 43

False

(penicillin can NOT)
(cephalosporin CAN)

Front 44

Cephalosporins should NEVER be administered at the same time as:

A. gentamicin
B. cycloserine
C. anti-histamines
D. anticoagulants

Back 44

A. gentamicin

(causes nephrotoxicity)

Front 45

T/F
Cephalosporins are contraindicated when a patient has a history of hypersensitivity to penicillin

Back 45

True

Front 46

Binds to PBPs, disrupting cell wall synthesis

A. Imipenem
B. azotreonam
C. Calvulanic acid
D. Sulbactam

Back 46

A. imipenem

Front 47

T/F

Imipenem has no risk if patient is allergic to penicillin

Back 47

False

Front 48

Interacts with PBP and induces formation of long filamentous bacteria
(select all)

A. Imipenem
B. azotreonam
C. Calvulanic acid
D. Sulbactam

Back 48

B. azotreonam

Front 49

T/F
Azotreonam has no activity against Gram – bacteria, and aerobic bacteria are resistant

Back 49

False

(no activity against GRAM +)
(ANAEROBIC bacteria are resistant)

Front 50

T/F
Patients allergic to penicillin can take azotreonam

Back 50

True

Front 51

Bind irreversibly with β-lactamase from both Gram + & Gram – bacteria; so known as "suicide" inhibitor of β-lactamase.
(select all)

A. imipenem
B. azotreonam
C. clavulanic acid
D. sulbactam

Back 51

C. clavulanic acid
D. sulbactam

Front 52

Binds terminal D-Ala-D-Ala of NAMA-NAG-carrier complex to inhibit cell wall polymerization

A. vancomycin
B. cycloserine
C. bacitracin
D. cephalosporin
E. penicillin

Back 52

A. Vancomycin

Front 53

_____ cells are resistant to vancomycin

A. Gram +
B. Gram –

Back 53

B. Gram –

(D-Ala-D-Ala replaced with D-Ala-D-ser or lactate)

Front 54

Used against mycobacteria

A. Vancomycin
B. cycloserine
C. bacitracin
D. cephalosporin
E. penicillin

Back 54

B. cycloserine

Front 55

Prevents addition of 2 terminal D-Ala by inhibiting alanine racemase & D-alaninyl-D-alanine synthetase

A. Vancomycin
B. cycloserine
C. bacitracin
D. cephalosporin
E. penicillin

Back 55

B. cycloserine

Front 56

Inhibits dephosphorylation of P-C55 lipid at the cell membrane

A. Vancomycin
B. cycloserine
C. bacitracin
D. cephalosporin
E. penicillin

Back 56

C. Bacitracin

Front 57

Why do antibiotic drugs not inhibit mammalian protein synthesis?

Back 57

Difference in ribosomal subunits

(Bacteria = 50S & 30S)
(Eukaryotes = 60S & 40S)

Front 58

T/F
Aminoglycosides are non-polar

Back 58

False

(highly polarized)

Front 59

____ have post-antibiotic effect which persists after the serum concentration, thus, keeps killing after the dosage stops

A. cephalosporins
B. penicillins
C. aminoglycosides
D. tetracyclines
E. chloramphenicols

Back 59

C. aminoglycosides

Front 60

List 3 ways aminoglycosides enter a cell

Back 60

1) diffuse through porins
2) Energy-Dependent Phase 1 (EDP1)
3) create fissure in bacteria, which enhances aminoglycoside uptake (EDP2)

Front 61

↓ pH, Ca²⁺/Mg²⁺, hyperosmolarity, and anaerobic conditions _____ entry/effectiveness of aminoglycosides

A. enhance
B. inhibit

Back 61

B. inhibit

Front 62

Describe how aminoglycosides prevent bacterial growth

Back 62

bind A site of 30S ribosome
↓
induce misread of mRNA
↓
premature termination
↓
causes polysomes to break up into monosomes

Front 63

Acetylation, phosphorylation, or adenylation of -OH or -NH2 groups of aminoglycosides _____ effectivenes.

A. enhance
B. inhibit

Back 63

B. inhibits

Front 64

Gentamycin can cause cross resistance to most aminoglycosides, except for:

A. tobramicin
B. amikamicin
C. kanamycin
D. netilmycin
E. streptomycin

Back 64

E. streptomycin

(much different structure than other aminoglycosides)

Front 65

The best way for aminoglycosides to be absorbed is

A. orally
B. rectally
C. IV
D. intramuscular
E. subcutaneous

Back 65

D. intramuscular

Front 66

T/F
Aminoglycosides can NOT cross placenta or BBB

Back 66

False

(CAN cross Placenta)
(can NOT cross BBB)

Front 67

Aminoglycosides are best used against:
(select all)

A. Aerobic
B. Anaerobic
C. Facultative anaerobic
D. Gram +
E. Gram –

Back 67

A. Aerobic
E. Gram –

(ANAEROBIC bacteria are RESISTANT)

Front 68

The first line drug for pseudomonas

A. aminoglycosides
B. cephalosporin
C. penicillin
D. tetracycline
E. chloramphenicol

Back 68

A. aminoglycosides

Front 69

Major side effects of aminoglycosides are:
(select all)

A. cell death of hair cells in hear (ototoxicity)
B. cell death of proximal tubules (nephrotoxicity)
C. cell death of hepatocytes (hepatotoxicity)
D. muscular blockade
E. teratogen

Back 69

A. cell death of hair cells in hear (ototoxicity)
B. cell death of proximal tubules (nephrotoxicity)
D. muscular blockade

Front 70

Which drugs lead to a loss of HIGH frequency tones (COCHLEAR damage)
(select all)

A. streptomycin
B. kanamycin
C. amikacin
D. gentamicin
E. neomycin
F. tobramycin

Back 70

B. kanamycin
C. amikacin
E. neomycin

Front 71

Which drugs lead to a loss of LOW frequency tones (VESTIBULAR damage)
(select all)

A. streptomycin
B. kanamycin
C. amikacin
D. gentamicin
E. neomycin
F. tobramycin

Back 71

A. streptomycin
D. gentamicin

Front 72

Rank the following drugs that are the greatest risk to MUSCULAR BLOCKADE

- kanamycin
- amikacin
- gentamicin
- neomycin
- tobramycin

Back 72

1) NEOMYCIN
- kanamycin
- amikacin
- gentamicin
- tobramycin

Front 73

Rank the following drugs that are the greatest risk to NEPHROTOXICITY

- streptomycin
- gentamicin
- neomycin
- tobramycin

Back 73

1) NEOMYCIN
- tobramycin
= gentamicin
- streptomycin

Front 74

Best used to treat tuberculosis and the plague

A. streptomycin
B. kanamycin
C. amikacin
D. gentamicin
E. neomycin
F. tobramycin

Back 74

A. streptomycin

Front 75

Should not be used against P. aeruginosa or Serratia
(select all)

A. streptomycin
B. kanamycin
C. amikacin
D. gentamicin
E. neomycin
F. tobramycin

Back 75

A. streptomycin
B. kanamycin

Front 76

1st aminoglycoside drug of choice

A. streptomycin
B. kanamycin
C. amikacin
D. gentamicin

Back 76

D. gentamicin

Front 77

Typically used in topical ointments

A. streptomycin
B. kanamycin
C. amikacin
D. gentamicin
E. neomycin

Back 77

E. neomycin

Front 78

Broadest spectrum aminoglycoside, which can be used to treat nosocomial Gram – infections

A. streptomycin
B. kanamycin
C. amikacin
D. gentamicin
E. neomycin

Back 78

C. amikacin

Front 79

Bind 30S ribosome to prevent protein synthesis
(select all)

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicols
E. penicillins

Back 79

A. aminoglycosides

(binds A site)

Front 80

Bind 50S ribosome to prevent protein synthesis
(select all)

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicols
E. penicillins

Back 80

B. macrolides (inhibits translocatoin to P site)
C. tetracyclines (binds A site)
D. chloramphenicols (inhibits peptidyltransferase)

Front 81

As a mechanism of resistance, some bacteria contain esterases which cleave the lactone ring of which antibiotic, rendering them inactive?

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicols
E. penicillins

Back 81

B. macrolides

Front 82

How do some bacteria use ribosomal protection as a mechanism of resistance against MACROLIDES?

Back 82

- mutation of 50S
- erm genes code for methylases

- both decrease drug binding

Front 83

T/F

Erythromycin is superior to Clarithromyin & Azithromycin in regards to absorption & acid stability

Back 83

False

(clarithromycin & azithromycin are superior to erythromycin)

(erythromycin is sensitive to acid)

Front 84

Erythromycin targets mostly ____ bacteria

A. Gram +
B. Gram –

Back 84

A. Gram +

(also Legionella & Mycoplasma)

Front 85

Erythromycin is found more in ____ than in ____

A. serum; tissue fluids
B. tissue fluids; serum

Back 85

A. serum; tissue fluids

Front 86

T/F

Erythromycin crosses placenta & enters mothers milk

Back 86

True

Front 87

Clarithromycin & azithromycin is found more in ____ than in ____

A. serum; tissue fluids
B. tissue fluids; serum

Back 87

B. tissue fluids; serum

Front 88

Which drug is superior against Gram + bacteria?

A. erythromycin
B. clarithromycin
C. azithromycin

Back 88

B. clarithromycin

Front 89

Which drug is superior against Gram – bacteria?

A. erythromycin
B. clarithromycin
C. azithromycin

Back 89

C. azithromycin

Front 90

What are the major adverse side effects of macrolides?
(select all)

A. hearing disturbances
B. Prolong QT interval (ventricular arrhythmia)
C. nephrotoxicity
D. pyloric stenosis in babies
E. cholestatic hepatitis

Back 90

A. hearing disturbances
B. Prolong QT interval (ventricular arrhythmia)
D. pyloric stenosis in babies (since macrolides cross placenta)
E. cholestatic hepatitis (mostly erythromycin)

Front 91

What is the major issue when taking erythromycin along with other drugs, such as:
- corticosteriods
- cyclosporin
- digoxin
- warfarin

Back 91

Inhibits CYP (in liver)
↓
decreases metabolism of those drugs
(which ↑ their concentration)

Front 92

T/F

Any macrolide can be used to treat chlamydial infections

Back 92

True

Front 93

Useful for respiratory tract infections for patients allergic to penicillins

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicols

Back 93

B. macrolides

Front 94

Match the mode of entry to the type of bacteria for tetracyclines
- passive diffusion via porins
- metabolic energy

A. Gram +
B. Gram –

Back 94

A. Gram + = metabolic energy
B. Gram – = passive diffusion via porins

Front 95

How do TETRACYCLINES exhibit antibiotic activity?

Back 95

Bind A site of 50S ribosome

Front 96

What are 3 ways bacteria build up resistance to tetracyclines?

Back 96

- antiporter system
- Erb enzymes
- R-protection protein
(dislodge tetracycline from ribosome)

Front 97

Induction of tetM imposes cross-resistance to:
(select all)

A. erythromycin
B. doxycycline
C. streptomycin
D. minocycline

Back 97

B. doxycycline
C. minocycline

Front 98

T/F

Tetracyclines can cross placenta and enter breast milk & CSF

Back 98

True

Front 99

T/F

Doxycycline CAN NOT be used in patients with impaired renal function

Back 99

False

(CAN be used)
(excreted in feces)

Front 100

Tetracyclines are more effective against _____ bacteria
(select all)
A. Gram +
B. Gram –
C. aerobic
D. anaerobic

Back 100

A. Gram +
D. anaerobic

Front 101

When can tetracycline staining occur in teeth?

Back 101

If taken during development of teeth

Front 102

Which drug is absorbed more completely?

A. minocycline
B. doxycycline

Back 102

A. minocycline

(mino = 100%)
(doxy = 95%)

(other tetracyclines not absorbed very well)

Front 103

Avoid dairy products when taking:

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicol
E. penicillins

Back 103

C. tetracyclines

(chelating agents impair absorption)

Front 104

How does chloramphenicol inhibit bacterial growth?

Back 104

- Binds 50S ribosome
- inhibits peptidyltransferase

Front 105

Can block mitochondrial protein synthesis in mammalian cells

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicol

Back 105

D. chloramphenicol

Front 106

Bacteria build up resistance against ____ via
- altering permeability of drug
- ribosomal mutation
- acetyl transferases

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicol

Back 106

D. chloramphenicol

Front 107

Bacteria build up resistance against ____ via
- ↓ permeability of drug
- modify ribosome binding site
- Group transferases (acetylation, phosphorylation, adenylation)

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicol

Back 107

A. aminoglycosides

Front 108

Bacteria build up resistance against ____ via
- efflux pumps
- ribosomal protection (methylases)
- esterases (cut lactone ring)

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicol

Back 108

B. macrolides

Front 109

Bacteria build up resistance against ____ via
- antiporter system
- R protection protein
- erb enzymes

A. aminoglycosides
B. macrolides
C. tetracyclines
D. chloramphenicol

Back 109

C. tetracyclines

Front 110

What are the major adverse side effects of chloramphenicol?

Back 110

- hematologic toxicity (gray baby syndrome)
- inhibits protein synthesis of mitochondrial membrane in mammalian cells

Front 111

What is the major issue when taking chloramphenicol along with other drugs, such as:

- warfarin
- dicumarol
- antiretroviral protease inhibitors

Back 111

- inhibits hepatic CYP

(INCREASES half-life of those drugs)

(Chlor alone = inhibits CYP)

Front 112

What is the major issue when taking chloramphenicol along with phenobarbital

Back 112

- activates hepatic CYP

(DECREASES half-life of chloramphenicol)

(Chlor + phenobarbital = activates CYP)

Front 113

What are the chelating agents for LEAD (Pb)?
(select all)

A. EDTA
B. dimercaptocccinate (succimer)
C. dimercaptopropanol (BAL, Dimercaprol)
D. Penicillamine
E. NAP
F. deferoxamine
G. Arsine gas

Back 113

A. EDTA
B. dimercaptocccinate (succimer)
C. dimercaptopropanol (BAL, Dimercaprol)
D. Penicillamine

Front 114

What are the chelating agents for MERCURY (Hg)?
(select all)

A. EDTA
B. dimercaptocccinate (succimer)
C. dimercaptopropanol (BAL, Dimercaprol)
D. Penicillamine
E. NAP
F. deferoxamine
G. Arsine gas

Back 114

B. dimercaptocccinate (succimer)
C. dimercaptopropanol (BAL, Dimercaprol)
D. Penicillamine
E. NAP

(NAP most effective)

Front 115

What are the chelating agents for CADMIUM (Cd)?
(select all)

A. EDTA
B. dimercaptocccinate (succimer)
C. dimercaptopropanol (BAL, Dimercaprol)
D. Penicillamine
E. NAP
F. deferoxamine
G. Arsine gas

Back 115

A. EDTA

Front 116

What are the chelating agents for ARSENIC (As)?
(select all)

A. EDTA
B. dimercaptocccinate (succimer)
C. dimercaptopropanol (BAL, Dimercaprol)
D. Penicillamine
E. NAP
F. deferoxamine
G. Arsine gas

Back 116

D. Penicillamine
E. NAP
G. Arsine gas (hemolytic agent)

Front 117

What are the chelating agents for IRON (Fe)?
(select all)

A. EDTA
B. dimercaptocccinate (succimer)
C. dimercaptopropanol (BAL, Dimercaprol)
D. Penicillamine
E. NAP
F. deferoxamine
G. Arsine gas

Back 117

F. deferoxamine

Front 118

What is the route of administration of dimercatopropanol (BAL, Dimercaprol)?

A. oral
B. IM
C. IV
D. SC
E. Transfusion

Back 118

B. IM

(in peanut oil)

Front 119

What is the route of administration of EDTA?

A. oral
B. IM
C. IV
D. SC
E. Transfusion

Back 119

C. IV

(as calcium disodium salt)

Front 120

What is the route of administration of Penicillamine?

A. oral
B. IM
C. IV
D. SC
E. Transfusion

Back 120

A. oral

Front 121

What is the route of administration of Deferoxamine?

A. oral
B. IM
C. IV
D. SC
E. Transfusion

Back 121

B. IM

(also slow IV)
(oral under rare circumstances)

Front 122

What is the route of administration of NAP?

A. oral
B. IM
C. IV
D. SC
E. Transfusion

Back 122

A. oral

Front 123

What is the route of administration of dimersuccinate (Succimerl)?

A. oral
B. IM
C. IV
D. SC
E. Transfusion

Back 123

A. oral

Front 124

What is the route of administration of arsine gas?

A. oral
B. IM
C. IV
D. SC
E. Transfusion

Back 124

E. transfusion

(arsine gas is a hemolytic agent)

Front 125

Why is EDTA given via IV?

A. more readily absorbed
B. cannot cross cell membrane
C. increased bioavailability
D. can't be activated in acidic environment

Back 125

B. cannot cross cell membrane

Front 126

T/F

EDTA only chelates circulating metal

Back 126

True

(because EDTA cannot enter inside the cell membrane)

Front 127

Why is EDTA given as a Calcium disodium salt?

A. to balance the sodium concentration
B. increases metal chelation
C. to act as an electron donor
D. to balance Calcium levels

Back 127

D. to balance Calcium levels

Front 128

What is the mechanism of LEAD toxicity?

A. inhibition of heme biosynthesis
B. inhibits α1-antitrypsin
C. precipitates proteins, necrosis of proximal tubule, and inhibits sulfhydryl (-SH) containing enzymes
D. Increases vascular permeability and inhibits anaerobic & oxidative phosphorylation

Back 128

A. inhibition of heme biosynthesis

(Diagnosed via d-aminolevulonic acid and Protoporphyrin IX
accumulation in plasma & urine)

Front 129

What is the mechanism of CADMIUM toxicity?

A. inhibition of heme biosynthesis
B. inhibits α1-antitrypsin
C. precipitates proteins, necrosis of proximal tubule, and inhibits sulfhydryl (-SH) containing enzymes
D. Increases vascular permeability and inhibits anaerobic & oxidative phosphorylation

Back 129

B. inhibits α1-antitrypsin

Front 130

What is the mechanism of MERCURY toxicity?

A. inhibition of heme biosynthesis
B. inhibits α1-antitrypsin
C. precipitates proteins, necrosis of proximal tubule, and inhibits sulfhydryl (-SH) containing enzymes
D. Increases vascular permeability and inhibits anaerobic & oxidative phosphorylation

Back 130

C. precipitates proteins, necrosis of proximal tubule, and inhibits sulfhydryl (-SH) containing enzymes

Front 131

What is the mechanism of ARSENIC toxicity?

A. inhibition of heme biosynthesis
B. inhibits α1-antitrypsin
C. precipitates proteins, necrosis of proximal tubule, and inhibits sulfhydryl (-SH) containing enzymes
D. Increases vascular permeability and inhibits anaerobic & oxidative phosphorylation

Back 131

D. Increases vascular permeability and inhibits anaerobic & oxidative phosphorylation

Front 132

Minamata disease is caused by toxic levels of:

A. lead
B. mercury
C. cadmium
D. arsenic
E. iron

Back 132

B. mercury

(from fish)
(study guide says from PLASTIC INDUSTRY)

Front 133

Pica is caused by toxic levels of:

A. lead
B. mercury
C. cadmium
D. arsenic
E. iron

Back 133

A. lead

(from children eating PAINT)

Front 134

How is lead toxicity diagnosed?

A. hair and fingernail results
B. dark colored gingival margins and palsy
C. increased levels of d-aminolevulonic acid & Protoporphyrin IX in plasma & urine
D. increased lead levels in plasma & urine
E. decreased heme levels

Back 134

C. increased levels of d-aminolevulonic acid & Protoporphyrin IX in plasma & urine

Front 135

Toxic levels of _____ have symptoms similar to emphysema, and are nephrotoxic

A. lead
B. mercury
C. cadmium
D. arsenic
E. iron

Back 135

C. cadmium

Front 136

This type of diabetes is due to B-cell destruction, causing an insulin deficiency

A. Type I
B. Type II
C. Type III
D. Type IV

Back 136

A. Type I

Front 137

This type of diabetes is due to a resistance to insulin action

A. Type I
B. Type II
C. Type III
D. Type IV

Back 137

B. Type II

Front 138

This type of diabetes is due to decreased pancreatic activity because of pancreatic disease, drug therapy, etc.

A. Type I
B. Type II
C. Type III
D. Type IV

Back 138

C. Type III

Front 139

This type of diabetes occurs during pregnancy (gestational diabetes)

A. Type I
B. Type II
C. Type III
D. Type IV

Back 139

D. Type IV

Front 140

What is the therapeutic target for FASTING glucose levels for a diabetic?

A. <140 mg/dL
B. <175 mg/dL
C. <100 mg/dL
D. <8%

Back 140

A. <140 mg/dL

Front 141

What is the therapeutic target for 2-hr POSTPRANDIAL (after eating) glucose levels for a Type I diabetic?

A. <140 mg/dL
B. <175 mg/dL
C. <100 mg/dL
D. <8%

Back 141

B. <175 mg/dL

Front 142

What is the therapeutic target for HbA-1c glucose levels for a diabetic?

A. <140 mg/dL
B. <175 mg/dL
C. <100 mg/dL
D. <8%

Back 142

D. <8%

Front 143

Type I diabetics take Rapid-acting, short-acting, intermediate-acting, and long-acting injections of insulin. They can also take oral drugs to restore blood glucose levels.

A. Both statements are true
B. Both statements are false
C. The first statement is true, the second statement is false
D. The first statement is false, the second statement is true

Back 143

C. The first statement is true, the second statement is false

(Type II diabetics take oral meds)

Front 144

T/F

Injectable and inhaled insulins are short-acting with rapid onset of action

Back 144

False

(they are Rapid-acting w/ Fast onset = genetically modified)

Front 145

T/F

Short-acting insulin with rapid onset of action are identical to endogenous insulin

Back 145

True

Front 146

Why use mixed insulin therapy?

Back 146

- provides a tighter glycemic control
- combines rapid & intermediate-acting insulins

Front 147

NPH + lispro/aspart/glulisine

A. stable premixed insulin
B. unstable premixed insulin

Back 147

B. unstable premixed insulin

Front 148

NPL + lispro insulin

A. stable premixed insulin
B. unstable premixed insulin

Back 148

A. stable premixed insulin

Front 149

NPA + aspart insulin

A. stable premixed insulin
B. unstable premixed insulin

Back 149

A. stable premixed insulin

Front 150

T/F

Administration of insulin glargine cannot be mixed with other types of insulin

Back 150

True

(due to acidic formulation)

Front 151

Can potentially cause hypoglycemia.
(select all)

A. hypoglycemic drugs
B. antihyperglycemic drugs

Back 151

A. hypoglycemic drugs

Front 152

Can not cause hypoglycemia.
(select all)

A. hypoglycemic drugs
B. antihyperglycemic drugs

Back 152

B. antihyperglycemic drugs

Front 153

Which group of drugs are hypoglycemic?
(select all)

A. Sulfonylureas
B. Biguanides
C. α-Glucosidase Inhibitors
D. Meglitinides
E. Thiazolidinediones

Back 153

A. Sulfonylureas
D. Meglitinides

Front 154

Which group of drugs are antihyperglycemic?
(select all)

A. Sulfonylureas
B. Biguanides
C. α-Glucosidase Inhibitors
D. Meglitinides
E. Thiazolidinediones

Back 154

B. Biguanides
C. α-Glucosidase Inhibitors
E. Thiazolidinediones

Front 155

How do SULFONYLUREAS treat Type II diabetes?

A. stimulate insulin secretion by blocking K⁺ channels
B. ligand of PPAR-γ nuclear receptor to increase lipid metabolism, insulin signaling, and adipocyte differentiation
C. block uptake of starch and disaccharides in upper GI
D. unclear mechanism

Back 155

A. stimulate insulin secretion by blocking K⁺ channels

Front 156

How do MEGLITINIDES treat Type II diabetes?

A. stimulate insulin secretion by blocking K⁺ channels
B. ligand of PPAR-γ nuclear receptor to increase lipid metabolism, insulin signaling, and adipocyte differentiation
C. block uptake of starch and disaccharides in upper GI
D. unclear mechanism

Back 156

A. stimulate insulin secretion by blocking K⁺ channels

Front 157

How do THIAZOLIDINEDIONES treat Type II diabetes?

A. stimulate insulin secretion by blocking K⁺ channels
B. ligand of PPAR-γ nuclear receptor to increase lipid metabolism, insulin signaling, and adipocyte differentiation
C. block uptake of starch and disaccharides in upper GI
D. unclear mechanism

Back 157

B. ligand of PPAR-γ nuclear receptor to increase lipid metabolism, insulin signaling, and adipocyte differentiation

Front 158

How do α-GLUCOSIDASE INHIBITORS treat Type II diabetes?

A. stimulate insulin secretion by blocking K⁺ channels
B. ligand of PPAR-γ nuclear receptor to increase lipid metabolism, insulin signaling, and adipocyte differentiation
C. block uptake of starch and disaccharides in upper GI
D. unclear mechanism

Back 158

C. block uptake of starch and disaccharides in upper GI

Front 159

How do BIGUANIDES treat Type II diabetes?

A. stimulate insulin secretion by blocking K⁺ channels
B. ligand of PPAR-γ nuclear receptor to increase lipid metabolism, insulin signaling, and adipocyte differentiation
C. block uptake of starch and disaccharides in upper GI
D. unclear mechanism

Back 159

D. unclear mechanism

Front 160

What are the major advantages of biguanides?
(select all)

A. prevents Type II diabetes in old age
B. prevents Type II diabetes in middle age
C. lower TG levels, and increase HDL
D. decrease hepatic glucose output & increase insulin sensitivity
E. Can be used in patients w/ allergy to sulfer drugs

Back 160

B. prevents Type II diabetes in middle age
D. decrease hepatic glucose output & increase insulin sensitivity

Front 161

What are the major advantages of thiazolidinediones?
(select all)

A. prevents Type II diabetes in old age
B. prevents Type II diabetes in middle age
C. lower TG levels, and increase HDL
D. decrease hepatic glucose output & increase insulin sensitivity
E. Can be used in patients w/ allergy to sulfer drugs

Back 161

C. lower TG levels, and increase HDL
D. decrease hepatic glucose output & increase insulin sensitivity

Front 162

What are the major advantages of Meglitinides?
(select all)

A. prevents Type II diabetes in old age
B. prevents Type II diabetes in middle age
C. lower TG levels, and increase HDL
D. decrease hepatic glucose output & increase insulin sensitivity
E. Can be used in patients w/ allergy to sulfer drugs

Back 162

E. Can be used in patients w/ allergy to sulfer drugs

Front 163

What are the major DISADVANTAGES of thiazolidinediones?
(select all)

A. contraindicated for patients w/ heart failure
B. alter bioavailability of oral contraceptives
C. may cause flatulence, diarrhea, and/or abdominal pain
D. contraindicated in alcoholics and patients w/ renal & hepatic disease
E. increased risk of lactic acidosis

Back 163

A. contraindicated for patients w/ heart failure
B. alter bioavailability of oral contraceptives

Front 164

What are the major DISADVANTAGES of sulfonylureas?
(select all)

A. contraindicated for patients w/ cardiovascular disease
B. alter bioavailability of oral contraceptives
C. may cause flatulence, diarrhea, and/or abdominal pain
D. contraindicated in alcoholics and patients w/ renal & hepatic disease
E. increased risk of lactic acidosis

Back 164

A. contraindicated for patients w/ cardiovascular disease

Front 165

What are the major DISADVANTAGES of biguanides?
(select all)

A. contraindicated for patients w/ cardiovascular disease
B. alter bioavailability of oral contraceptives
C. may cause flatulence, diarrhea, and/or abdominal pain
D. contraindicated in alcoholics and patients w/ renal & hepatic disease
E. increased risk of lactic acidosis

Back 165

D. contraindicated in alcoholics and patients w/ renal & hepatic disease
E. increased risk of lactic acidosis

Front 166

What are the major DISADVANTAGES of α-glucosidase inhibitors?
(select all)

A. contraindicated for patients w/ heart failure
B. alter bioavailability of oral contraceptives
C. may cause flatulence, diarrhea, and/or abdominal pain
D. contraindicated in alcoholics and patients w/ renal & hepatic disease
E. increased risk of lactic acidosis

Back 166

C. may cause flatulence, diarrhea, and/or abdominal pain

Front 167

Which of the following ↑ insulin secretion, but may cause hypoglycemia?
(select all)

A. Sulfonylureas
B. Biguanides
C. α-Glucosidase Inhibitors
D. Meglitinides
E. Thiazolidinediones
F. Enteroglucagons

Back 167

A. Sulfonylureas
D. Meglitinides
F. Enteroglucagons

Front 168

Which of the following ↓ hepatic glucose output & ↑ insulin sensitivity?

A. Sulfonylureas
B. Biguanides
C. α-Glucosidase Inhibitors
D. Meglitinides
E. Thiazolidinediones
F. Enteroglucagons

Back 168

B. Biguanides (Metformin)
E. Thiazolidinediones

Front 169

Which of the following are 1st line drugs for Type II diabetes?

A. Sulfonylureas
B. Biguanides
C. α-Glucosidase Inhibitors
D. Meglitinides
E. Thiazolidinediones
F. Enteroglucagons

Back 169

A. Sulfonylureas
B. Biguanides (Metformin)

Front 170

Act primarily by direct effects on the Chemoreceptor Trigger Zone

A. proemetic drugs
B. antiemetic drugs
C. prokinetic agents
D. antidiarrheal agents
E. laxatives and cathartics

Back 170

A. proemetic drugs

Front 171

Used in cases of oral poisoning

A. proemetic drugs
B. antiemetic drugs
C. prokinetic agents
D. antidiarrheal agents
E. laxatives and cathartics

Back 171

A. proemetic drugs

Front 172

Used for motion sickness, postoperative nausea, and nausea due to chemotherapy/radiation

A. proemetic drugs
B. antiemetic drugs
C. prokinetic agents
D. antidiarrheal agents
E. laxatives and cathartics

Back 172

B. antiemetic drugs

Front 173

Ineffective against chemotherapy-induced nausea

A. anticholinergic drug
B. cannabinoids
C. D2 dopamine antagonists
D. H1 antihistamine drugs
E. 5HT3 serotonin antagonists

Back 173

D. H1 antihistamine drugs

Front 174

Used to treat gastroparesis (lack of GI motility)

A. proemetic drugs
B. antiemetic drugs
C. prokinetic agents
D. antidiarrheal agents
E. laxatives and cathartics

Back 174

C. prokinetic drugs

Front 175

Used against postoperative GI paralysis, diabetic gastroparesis, and GERD

A. proemetic drugs
B. antiemetic drugs
C. prokinetic agents
D. antidiarrheal agents
E. laxatives and cathartics

Back 175

C. prokinetic drugs

Front 176

Metoclopramide is an antiemetic, whose primary effect is a 5HT4 (serotonin) antagonist; and it's secondary effect is as a D2 agonist

A. Both statements are true
B. Both statements are false
C. The first statement is true, the second statment is false
D. The first statement is false, the second statement is true

Back 176

B. Both statements are false

(5HT4 AGONIST = prokinetic effect)
(D2 ANTAGONIST = antiemetic effect)

Front 177

T/F

Macrolides can be used for diabetic gastroparesis

Back 177

True

(erythromycin)

Front 178

Increase stool viscosity and absorb water

A. proemetic drugs
B. antiemetic drugs
C. prokinetic agents
D. antidiarrheal agents
E. laxatives and cathartics

Back 178

D. antidiarrheal agents

Front 179

Increase stool volume or decrease transit time

A. proemetic drugs
B. antiemetic drugs
C. prokinetic agents
D. antidiarrheal agents
E. laxatives and cathartics

Back 179

E. laxatives and cathartics

Front 180

Which of the following antidiarrheal agents have are opioid which have a significant CNS effect?
(select all)

A. bismuth salycilate
B. loperamide
C. diphenoxylate
D. difenoxin
E. octreotide

Back 180

C. diphenoxylate
D. difenoxin

(Loperamide is antidiarrheal with minimal CNS effect)

Front 181

Retain water & support bacterial growth

A. "bulk" laxatives
B. "saline" laxatives
C. nondigestible sugars & alcohols
D. stimulant laxatives

Back 181

A. "bulk" laxatives

Front 182

Non-absorbable inorganic salts, which create a hyperosmotic luminal environment to increase secretion & decrease reabsorption

A. "bulk" laxatives
B. "saline" laxatives
C. nondigestible sugars & alcohols
D. stimulant laxatives

Back 182

B. "saline" laxatives

Front 183

Directly stimulate colonic motility & enhance secretion of fluid & electrolytes

A. "bulk" laxatives
B. "saline" laxatives
C. nondigestible sugars & alcohols
D. stimulant laxatives

Back 183

D. stimulant laxatives

Front 184

Weak inorganic bases that neutralize stomach acid and raise pH

A. antacids
B. H2 receptor antagonists
C. proton pump inhibitors
D. prostaglandins and protective agents

Back 184

A. antacids

Front 185

T/F

Antacids are useful for chronic disorders of gastric acid secretion

Back 185

False

(Not effective vs chronic)

Front 186

Block stimulation of parietal cell activity by histamine

A. antacids
B. H2 receptor antagonists
C. proton pump inhibitors
D. prostaglandins and protective agents

Back 186

B. H2 receptor antagonists

Front 187

Which of the following H2 receptor antagonists is a potent inhibitor of CYP3A4?

A. cimetidine
B. ranitidine
C. famotidine
D. nizatidine

Back 187

A. cimetidine (TAGAMET)

Front 188

Acts directly on proton pumps by covalently & irreversibly deactivating them.

A. antacids
B. H2 receptor antagonists
C. proton pump inhibitors
D. prostaglandins and protective agents

Back 188

C. proton pump inhibitors

Front 189

Inhibits acid secretion & promotes mucus and bicarbonate secretion

A. antacids
B. H2 receptor antagonists
C. proton pump inhibitors
D. prostaglandins and protective agents

Back 189

D. prostaglandins & protective agents

Front 190

H. pylorii infection is an important etiological factor for:

A. Peptic Ulcer Disease (PUD)
B. GERD

Back 190

A. PUD

Front 191

Lack of esophageal motility & tone of the esophageal sphincter is an important factor for:

A. Peptic Ulcer Disease (PUD)
B. GERD

Back 191

B. GERD

Front 192

T/F

The most effective treatment for PUD & GERD involve multiple therapeutic approaches

Back 192

True

(Proton pump inhibitors + H2 receptor antagonists)

Front 193

Used to treat INFLUENZA
(select all)

A. amantadine
B. acyclovir
C. ganciclovir
D. zidovudine (AZT)
E. rimantadine
F. saquinavir
G. nevirapine

Back 193

A. amantadine
E. rimantadine

Front 194

Used to treat HERPES
(select all)

A. amantadine
B. acyclovir
C. ganciclovir
D. zidovudine (AZT)
E. rimantadine
F. saquinavir
G. nevirapine

Back 194

B. acyclovir
C. ganciclovir

Front 195

Used to treat HIV
(select all)

A. amantadine
B. acyclovir
C. ganciclovir
D. zidovudine (AZT)
E. rimantadine
F. saquinavir
G. nevirapine

Back 195

D. zidovudine (AZT) = NRTI
F. saquinavir = Protease Inhibitor
G. nevirapine = NNRTI

Front 196

Which of the following antiviral drugs is/are NOT analog(s) of nucleosides?
(select all)

A. amantadine
B. rimantadine
C. acyclovir
D. foscarnet
E. vidarabine

Back 196

D. foscarnet

Front 197

Why are nucleoside analogs used as antiviral agents?

Back 197

Converted into triphosphate analog
↓
competes w/ native nucleoside for incorporation into viral DNA
↓
inhibits viral DNA polymerase
↓
DNA chain termination

Front 198

Which of the following are ESTER local anesthetics?
(select all)

A. Mepivacaine
B. Tetracaine
C. Benzocaine
D. Cocaine
E. Bupivacaine
F. Lidocaine
G. Procaine

Back 198

B. Tetracaine
C. Benzocaine
D. Cocaine
G. Procaine

Front 199

Which of the following are AMIDE local anesthetics?
(select all)

A. Mepivacaine
B. Tetracaine
C. Benzocaine
D. Cocaine
E. Bupivacaine
F. Lidocaine
G. Procaine

Back 199

A. Mepivacaine
E. Bupivacaine
F. Lidocaine

Front 200

At rest, a neuronal cell contains more open K⁺ channels. Thus K⁺ can flow outside of the cell, creating a negative concentration gradient.

A. Both statements are true
B. Both statements are false
C. The first statement is true, the second statement is false
D. The first statement is false, the second statement is true

Back 200

A. Both statements are true

Front 201

Describe nerve conduction

Back 201

Depolarization opens Na⁺ channels
↓
Na⁺ flows into cell
↓
Na⁺ channels close & K⁺ channels open
↓
K⁺ exits cell
↓
membrane returns to rest
↓
Depolarization of nearby Na⁺ channels causes propagation along axon

Front 202

The ester or amide of a local anesthetic is part of the ____ of it's structure

A. hydrophobic group (lipophilic)
B. intermediate chain
C. ionizable group (amine substitute)

Back 202

B. intermediate chain

Front 203

Local anesthetics are ______

A. weak acids
B. strong acids
C. weak bases
D. strong bases

Back 203

C. weak bases

Front 204

The _____ form of local anesthetics are more lipophilic (more rapidly diffuse through membrane), while the _____ form has higher affinity for the Na⁺ channel

A. charged; uncharged
B. uncharged; charged

Back 204

B. uncharged; charged

Front 205

Which local anesthetic has a longer half-life?

A. amide-linked
B. ester-linked

Back 205

A. amide-linked

Front 206

Quickly hydrolyzed by enzymes in the blood

A. amide-linked anesthetics
B. ester-linked anesthetics

Back 206

B. ester-linked anesthetics

Front 207

Widely distributed via the circulation and are hydrolyzed in the liver

A. amide-linked anesthetics
B. ester-linked anesthetics

Back 207

A. amide-linked anesthetics

Front 208

What are 4 reasons why vasoconstrictors are added to the local anesthetic preparations?

Back 208

1. reduce absorption of LA
2. enhance drug concentration
3. prolong LA effect
4. reduce blood LA levels (↓ toxicity)

Front 209

Local anesthetic toxicity often causes _____ of the CNS

A. stimulation
B. depression

Back 209

A. stimulation

(high levels can cause depression & respiratory failure)

Front 210

Local anesthetic toxicity often causes _____ in the activity of the heart

A. stimulation
B. depression

Back 210

B. depression

Front 211

Local anesthetic toxicity often causes _____

A. vasodilation
B. vasoconstriction

Back 211

A. vasodilation

(Cocaine = vasoconstriction)

Front 212

_____ is the most cardiotoxic local anesthetic

A. lidocaine
B. procaine
C. mepivacaine
D. bupivacaine
E. cocaine

Back 212

D. bupivacaine

(cardiovascular collapse & ventricular tachycardia)

Front 213

Which of the following antineoplastic drugs do NOT cause bone marrow suppression?
(select all)

A. methotrexate
B. vincristine
C. asparginase
D. 5-fluorouracil
E. daunorubicin
F. bleomycin

Back 213

B. vincristine
C. asparaginase
F. bleomycin

Front 214

How do ALKYLATING AGENTS exhibit their cytotoxicity?
(select all)

A. Inhibit formation of FH4 from folic acid by inhibiting DHFR, thereby blocking DNA synthesis
B. cleaves DNA & inhibits repair
C. Block thymidine synthesis or incorporated into DNA to interfere w/ DNA synthesis
D. binds & inhibits tubulin, disrupting microtubule of cytoskeleton & mitotic spindle
E. intercalates with DNA to blocks topoisomerase
F. cross-linking of Guanine nucleobases causing inhibition of DNA synthesis

Back 214

F. cross-linking of Guanine nucleobases causing inhibition of DNA synthesis

Front 215

How do NATURAL PRODUCTS exhibit their cytoxicity?
(select all)

A. Inhibit formation of FH4 from folic acid by inhibiting DHFR, thereby blocking DNA synthesis
B. cleaves DNA & inhibits repair
C. Block thymidine synthesis or incorporated into DNA to interfere w/ DNA synthesis
D. binds & inhibits tubulin, disrupting microtubule of cytoskeleton & mitotic spindle
E. intercalates with DNA to blocks topoisomerase
F. cross-linking of Guanine nucleobases causing inhibition of DNA synthesis

Back 215

B. cleaves DNA & inhibits repair (bleomycin)

D. binds & inhibits tubulin, disrupting microtubule of cytoskeleton & mitotic spindle (vincristine & vinblastine)

E. intercalates with DNA to blocks topoisomerase (daunoribicin & doxorubicin)

Front 216

How do ANTIMETABOLITES exhibit their cytoxicity?
(select all)

A. Inhibit formation of FH4 from folic acid by inhibiting DHFR, thereby blocking DNA synthesis
B. cleaves DNA & inhibits repair
C. Block thymidine synthesis or incorporated into DNA to interfere w/ DNA synthesis
D. binds & inhibits tubulin, disrupting microtubule of cytoskeleton & mitotic spindle
E. intercalates with DNA to blocks topoisomerase
F. cross-linking of Guanine nucleobases causing inhibition of DNA synthesis

Back 216

A. Inhibit formation of FH4 from folic acid by inhibiting DHFR, thereby blocking DNA synthesis
(methotrexate)

C. Block thymidine synthesis or incorporated into DNA to interfere w/ DNA synthesis
(5-fluorouracil)

Front 217

How does CISPLATIN exhibit their cytoxicity?
(select all)

A. Inhibit formation of FH4 from folic acid by inhibiting DHFR, thereby blocking DNA synthesis
B. cleaves DNA & inhibits repair
C. Block thymidine synthesis or incorporated into DNA to interfere w/ DNA synthesis
D. binds & inhibits tubulin, disrupting microtubule of cytoskeleton & mitotic spindle
E. intercalates with DNA to blocks topoisomerase
F. cross-linking of Guanine nucleobases causing inhibition of DNA synthesis

Back 217

F. cross-linking of Guanine nucleobases causing inhibition of DNA synthesis

Front 218

Affect only proliferating tissues and require intact DNA repair pathway to trigger cell death, such as p53.

A. alkylating agents
B. natural products
C. aminometabolites

Back 218

A. alkylating agents

Front 219

How do cancer cells build a resistance to ALKYLATING AGENTS?

A. impair enzymatic activity required for activation
B. impair transport into the cell
C. decreased transport & increased metabolism

Back 219

C. decreased transport (melphalan) & increased metabolism

Front 220

How do cancer cells build a resistance to METHOTREXATE (antimetabolite)?

A. impair enzymatic activity required for activation
B. impair transport into the cell
C. decreased transport & increased metabolism

Back 220

B. impair transport into the cell

(folic acid analog)

Front 221

How do cancer cells build a resistance to 5-FLUOROURACIL (antimetabolite)?

A. impair enzymatic activity required for activation
B. impair transport into the cell
C. decreased transport & increased metabolism

Back 221

A. impair enzymatic activity required for activation

(pyrimidine analog - uracil)

Front 222

How do cancer cells build a resistance to CYTARABINE (antimetabolite)?

A. impair enzymatic activity required for activation
B. impair transport into the cell
C. decreased transport & increased metabolism

Back 222

A. impair enzymatic activity required for activation

(cytidine analog)

Front 223

Hormonal treatment for breast cancer (before & after surgery/radiation)

A. actinomycin D
B. tamoxifen
C. cisplatin
D. melphalan

Back 223

B. tamoxifen

Front 224

What are 3 main reasons cancer cells develop resistance to drug treatment

Back 224

1. loss of p53 function
2. loss of DNA mismatch repair (MMR)
3. ↑ multi-drug resistance (MDR1) gene expression (↑ drug efflux)

Front 225

The antimicrobial action of Cefapime and Amoxicillin involve which of the following mechanisms?
(select all)

A. inhibit transpeptidase
B. prevents cleavage of sugar-peptide from the lipid carrier
C. interferes w/ formation of initial complex for peptide formation
D. inhibits formation of D-alanyl-D-alanine dipeptide
E. interferes w/ cell wall synthesis

Back 225

A. inhibit transpeptidase
E. interferes w/ cell wall synthesis

Front 226

The antimicrobial action of bacitracin involves which of the following mechanisms?
(select all)

A. inhibit transpeptidase
B. prevents cleavage of sugar-peptide from the lipid carrier
C. interferes w/ formation of initial complex for peptide formation
D. inhibits formation of D-alanyl-D-alanine dipeptide
E. interferes w/ cell wall synthesis

Back 226

B. prevents cleavage of sugar-peptide from the lipid carrier
E. interferes w/ cell wall synthesis

Front 227

The antimicrobial action of gentamicin and streptomycin involve which of the following mechanisms?
(select all)

A. inhibit transpeptidase
B. prevents cleavage of sugar-peptide from the lipid carrier
C. interferes w/ formation of initial complex for peptide formation
D. inhibits formation of D-alanyl-D-alanine dipeptide
E. interferes w/ cell wall synthesis

Back 227

C. interferes w/ formation of initial complex for peptide formation

(aminoglycosides block 30S A-site)

Front 228

The antimicrobial action of cycloserine involve which of the following mechanisms?
(select all)

A. inhibit transpeptidase
B. prevents cleavage of sugar-peptide from the lipid carrier
C. interferes w/ formation of initial complex for peptide formation
D. inhibits formation of D-alanyl-D-alanine dipeptide
E. interferes w/ cell wall synthesis

Back 228

D. inhibits formation of D-alanyl-D-alanine dipeptide
E. interferes w/ cell wall synthesis

Front 229

A serious toxicity associated w/ penicillin is:
(select all)

A. hypersensitivity
B. photosensitivity
C. scalded skin syndrome
D. anemia
E. renal tubular necrosis
F. tooth discoloration
G. hearing loss

Back 229

A. hypersensitivity

Front 230

A serious toxicity associated w/ tetracyclines is:
(select all)

A. hypersensitivity
B. photosensitivity
C. scalded skin syndrome
D. anemia
E. renal tubular necrosis
F. tooth discoloration
G. hearing loss

Back 230

B. photosensitivity
F. tooth discoloration

Front 231

A serious toxicity associated w/ aminoglycosides is:
(select all)

A. hypersensitivity
B. photosensitivity
C. scalded skin syndrome
D. anemia
E. renal tubular necrosis
F. tooth discoloration
G. hearing loss

Back 231

E. renal tubular necrosis
G. hearing loss

Front 232

Which of the following statements regarding Gentamicin are FALSE
(select all)

A. can produce non-competitive blockage of nicotinic receptors at neuromuscular junctions
B. useful against Gram –, anaerobic bacteria
C. Induce hearing loss
D. readily penetrate the CNS
E. administered safely to patients w/ renal failure

Back 232

B. useful against Gram –, anaerobic bacteria
(useful against Gram –, AEROBIC bacteria)

E. administered safely to patients w/ renal failure
(aminoglycosides cause renal tubular necrosis)

Front 233

Streptomycin impairs bacterial growth by which of the following procedures:
(select all)

A. inhibits transpeptidase engaged in cell wall synthesis
B. inhibits binding of aa-tRNA to 30S ribosome
C. breakdown of polysomes
D. increased permeability of cell wall resulting in lysis of the organism
E. binding of drug to protein in the cell membrane

Back 233

B. inhibits binding of aa-tRNA to 30S ribosome
C. breakdown of polysomes
E. binding of drug to protein in the cell membrane ("partially correct")