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Chapter 14 Trivia

Total questions: 46

Worksheet time: 37mins

Name
Class
Date
1.

Which is NOT an example of how antimicrobials have been used historically?

a)

Beer was made by fermenting a tetracycline-producing bacteria.

b)

Indian and Chinese herbalist used plants with antibiotic properties.

c)

Many cultures have taken advantage of antimicrobial properties of fungi.

d)

Ancient Greeks isolated penicillin from a mold to treat wounds.

2.

What disease was the first to be cured using a systemically identified chemical agent called Compound 606?

a)

influenza

b)

syphilis

c)

tuberculosis

d)

pneumonia

3.

What was the first natural antibiotic discovered by Alexander Fleming?

a)

rifampin

b)

tetracycline

c)

penicillin

d)

ampicillin

4.

Which is NOT one of the natural antibiotics isolated from soil by Selman Waksman?

a)

actinomycin

b)

streptomycin

c)

amoxicillin

d)

neomycin

5.

What was the first synthetic antibiotic, which was developed by Gerhard Domagk and colleagues?

a)

sulfanilamide

b)

methicillin

c)

vancomycin

d)

polymyxin

6.

What is the source of many of the world’s natural antibiotics in use today?

a)

soil

b)

human gut

c)

tropical plants

d)

aquatic organisms

7.

Which of the following is most important when deciding to treat with a bacteriostatic versus bactericidal drug?

a)

whether the drug can be administered orally or intravenously

b)

whether the drug is natural or synthetic

c)

whether the pathogen is gram-positive or gram-negative

d)

whether the patient has a strong immune system

8.

When would a narrow-spectrum antimicrobial be used?

a)

for a polymicrobic infection

b)

when the infecting pathogen has been identified

c)

to prevent infection during surgery

d)

when the pathogen has developed resistance to a broad-spectrum antibiotic

9.

What is a major risk associated with broad-spectrum antimicrobials?

a)

superinfections

b)

heart failure

c)

neurotoxicity

d)

cancer

10.

What is a common reason to use an antibiotic with a shorter half-life?

a)

To minimize side effects of a particular drug

b)

To decrease the number of doses needed per day

c)

To allow the drug to be taken orally

d)

To more effectively treat a chronic infection

11.

What type of drug is more effective when taken in smaller doses over a long period of time?

a)

dose-dependent drug

b)

chronic drug

c)

time-dependent drug

d)

acute drug

12.

Which route of administration achieves the quickest response time and highest plasma levels?

a)

topical

b)

oral

c)

intramuscular

d)

intravenous

13.

When might oral administration of a drug be ineffective?

a)

when the patient has been vomiting

b)

when low levels of drugs are needed over a long time period

c)

when the drug tends to be toxic at higher plasma levels

d)

when the patient has kidney dysfunction

14.

What is an example of a synergistic drug interaction?

a)

an antibiotic decreases the effectiveness of a contraceptive

b)

an antacid blocks absorption of a drug into the GI

c)

two antibiotics are bactericidal in combination but bacteriostatic individually

d)

two drugs have reduced effectiveness when used together

15.

What is selective toxicity?

a)

An antibiotic kills/inhibits growth of bacteria without harming the host.

b)

An antibiotic is more effective against gram+ than gram- bacteria.

c)

An antibiotic is toxic to the host at only high concentrations.

d)

An antibiotic only works under certain environmental conditions.

16.

How do β-lactams inhibit cell wall synthesis?

a)

block export of peptidoglycans out of cell

b)

block crosslinking of peptidoglycans

c)

block assembly of glucose units into cellulose

d)

block synthesis of glucose units needed for cellulose synthesis

17.

Would Gram+ or Gram- bacteria be more sensitive to drugs that inhibit cell wall synthesis?

a)

Gram +

b)

Gram -

18.

What step in cell wall synthesis is blocked by glycopeptides?

a)

export of peptidoglycan units from the cell

b)

crosslinking of peptides between peptidoglycan units

c)

addition of peptides to NAM units

d)

assembly of NAG and NAM units

19.

What step in cell wall synthesis is blocked by bacitracin?

a)

export of peptidoglycan units from the cell

b)

crosslinking of peptides between peptidoglycan units

c)

addition of peptides to NAM units

d)

assembly of NAG and NAM units

20.

How are protein synthesis-inhibiting antibiotics selectively toxic?

a)

The eukaryotic RNA polymerase is structurally different from prokaryotic.

b)

Eukaryotes do not need to synthesize proteins.

c)

The eukaryotic ribosome is structurally different from prokaryotic.

d)

Eukaryotes use a completely different mechanism to synthesize proteins.

21.

Which bacteria are more effectively targeted by inhibitors of membrane function?

a)

Gram +

b)

Gram -

22.

What enzyme is the target of fluoroquinolones?

a)

RNA polymerase

b)

Transpeptidase

c)

DNA polymerase

d)

DNA gyrase

23.

Which is NOT a type of antibiotic often used to treat tuberculosis?

a)

RNA synthesis inhibitor

b)

mycolic acid synthesis inhibitor

c)

ATP synthase inhibitor

d)

folic acid synthesis inhibitor

24.

How do sulfonamides and trimethoprim work as bacteriostatic agents?

a)

block DNA replication

b)

block cell wall synthesis

c)

block folic acid synthesis

d)

block ATP synthesis

25.

Why is it difficult to find or develop antimicrobials against fungi, protozoa, and helminths?

a)

There are fewer targets for selective toxicity.

b)

There are fewer drugs that can damage them.

c)

They are more resilient than prokaryotes.

d)

They are too complicated to design effective drugs.

26.

What molecule is the most common target of antifungal drugs?

a)

DNA gyrase

b)

chitin

c)

peptidoglycan

d)

ergosterol

27.

Which biomolecule is a common target of antifungal drugs?

a)

chitin

b)

peptidoglycan

c)

cellulose

d)

keratin

28.

How does flucytosine, a pyrimidine analog, inhibit the growth of fungi?

a)

interferes with DNA replication

b)

blocks mitochondrial function

c)

interferes with microtubule spindle formation

d)

blocks chitin synthesis

29.

Which is an antifungal target that functions in cell division?

a)

ergosterol

b)

kDNA

c)

β(1→3) glucans

d)

microtubules

30.

Which drug interferes with the electron transport chain in both fungal and protozoan mitochondria?

a)

fluoroquinolone

b)

atovaquone

c)

penicillin

d)

acyclovir

31.

Which is NOT a mechanism used by antiprotozoan drugs?

a)

produce ROS that damage macromolecules

b)

inhibit folic acid synthesis

c)

blocks electron transport chain

d)

interferes with ergosterol synthesis

32.

What structure is unique to trypanosomes (a type of protozoa) and is a good selectively toxic target?

a)

kinetoplasts (kDNA)

b)

mitotic spindles

c)

β(1→3) glucans

d)

DNA gyrase

33.

Which is NOT a mechanism of action of antihelminthic drugs?

a)

blocks neuronal transmission

b)

inhibits oxidative phosphorylation

c)

prevents mycolic acid synthesis

d)

causes an influx of calcium

34.

Avermectins, which are neurotoxic to helminths, ultimately kill them through which mechanism?

a)

cause the worms to swell and burst

b)

cause paralysis and starvation

c)

blocks cellular respiration

d)

creates breaks in DNA that kill individual cells

35.

Which drug is would be effective against protozoa, fungi, viruses, and cancer cells?

a)

pentamidine, which cleaves kDNA

b)

avermectins, which block neuronal transmission

c)

nikkomycin, which blocks chitin synthesis

d)

benzimidazoles, which interfere with microtubule function

36.

Which is NOT a factor that allows microorganisms to acquire drug resistance

a)

inappropriate use or overuse of antimicrobials

b)

subtherapeutic dosing

c)

allowing patient immune systems to fight minor infections without drugs

d)

patient noncompliance with completing treatment

37.

What is an example of resistance through drug modification?

a)

decrease in the amount of porin for carbapenem entry

b)

glycosylation of rifampin blocks binding to target

c)

adding a chemical group to RNA polymerase

d)

the microbe produces a molecule that mimics DNA structure

38.

Which is NOT a way in which a cell can limit the amount of drug reaching its intracellular target?

a)

breaking down the cell wall

b)

decreasing the number of porin channels

c)

increasing the number of efflux pumps

d)

changes in outer membrane lipid composition

39.

What is a very common mechanism of resistance that can be easily achieved by spontaneous mutations?

a)

drug inactivation

b)

enzymatic bypass

c)

target modification

d)

prevention of cellular uptake

40.

What is a mechanism of resistance to antimicrobials that target metabolic pathways?

a)

Cross-linkage in the cell wall is decreased.

b)

The microbe overproduces the target enzyme.

c)

The microbe improves DNA repair pathways.

d)

Efflux pumps in the cell membrane are increased.

41.

What is an example of target mimicry?

a)

decrease in the amount of porin for carbapenem entry

b)

glycosylation of rifampin blocks binding to target

c)

adding a chemical group to RNA polymerase

d)

the microbe produces a molecule that is similar in structure to DNA

42.

What is a “superbug”?

a)

a microbe with resistance to multiple antimicrobials

b)

a microbe the grows at an extremely elevated rate

c)

a very large microbe

d)

a microbe that spreads between people easily

43.

What does cross-resistance mean?

a)

A microbe has multiple mechanisms of resistance to one antimicrobal.

b)

Two microbes are resistant to the same antimicrobial.

c)

One mechanism allows resistance to multiple antimicrobials.

d)

An antimicrobial can affect both prokaryotes and eukaryotes.

44.

By what mechanism has MRSA become resistant to methicillin?

a)

acquisition a PBP with low-affinity to β-lactams

b)

structural change to the peptide component of peptidoglycans

c)

production of a β-lactamase enzyme

d)

active efflux of carbapenems out of the cell

45.

Which is NOT one of the clinically relevant vancomycin-resistant strains?

a)

VISA

b)

VRE

c)

VRSA

d)

VIE

46.

Which is NOT a drug that ESBLs are resistant to?

a)

monobactams

b)

cephalosporins

c)

carbapenems

d)

penicillins