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Aminoglycosides

Total questions: 77

Worksheet time: 39mins

Name
Class
Date
1.

Which of the following is true about aminoglycosides?

a)

They contain 1 or 2 amino-sugar units linked to a central sugar nucleus.

b)

They were first discovered in 1943 from the soil microbe Streptomyces.

c)

They attack aerobic Gram-negative bacteria.

d)

All of the above.

2.

Fill in the blank: The aminoglycoside antibiotic that was designed to be resistant to enzymes used by bacteria to deactivate aminoglycoside antibiotics is _________.

a)

amikacin

b)

gentamicin

c)

streptomycin

d)

tobramycin

3.

Which disease is a 'claim to fame' for aminoglycosides due to their effectiveness?

a)

Tuberculosis

b)

Influenza

c)

Malaria

d)

Diabetes

4.

Two examples of aminoglycoside antibiotics are:

a)

Gentamicin and Amikacin

b)

Penicillin and Amoxicillin

c)

Ciprofloxacin and Levofloxacin

d)

Vancomycin and Teicoplanin

5.

What is the main target of aminoglycosides in bacterial cells?

a)

50S rRNA

b)

30S rRNA

c)

DNA polymerase

d)

Cell wall

6.

The mechanism of action (MOA) of aminoglycosides is well understood.

a)

True

b)

False

7.

Fill in the blank: Abnormal initiation complexes or misreading of the ______ template can lead to the incorporation of incorrect amino acids during protein synthesis.

a)

mRNA

b)

tRNA

c)

DNA

d)

rRNA

8.

Fluoroquinolones were discovered in which type of study?

a)

Viral

b)

Fungal

c)

Malarial

d)

Bacterial

9.

Fluoroquinolones are fully synthetic and broad spectrum antibiotics effective against which types of bacteria?

a)

Gram positive only

b)

Gram negative only

c)

Gram positive and Gram negative

d)

None of the above

10.

Fill in the blank: The 2nd generation fluoroquinolone is ________ (Cipro).

a)

Ciprofloxacin

b)

Levofloxacin

c)

Moxifloxacin

d)

Norfloxacin

11.

Which generation of fluoroquinolones does levofloxacin (Levaquin) belong to?

a)

1st

b)

2nd

c)

3rd

d)

4th

12.

Fluoroquinolones distribute to ________ fluid, so they can be used to treat meningitis.

a)

cerebrospinal

b)

synovial

c)

pleural

d)

peritoneal

13.

What is the main mechanism of action of fluoroquinolones?

a)

Inhibit cell wall synthesis

b)

Prevent replication and repair of bacterial DNA & RNA

c)

Inhibit protein synthesis

d)

Disrupt cell membrane

14.

Fill in the blank: DNA gyrase is responsible for the supercoiling of ______ double.

a)

DNA

b)

RNA

c)

Protein

d)

Lipid

15.

What class of drugs are sulfanilamides also known as?

a)

Beta-lactams

b)

Sulfa drugs

c)

Macrolides

d)

Tetracyclines

16.

Fill in the blank: Sulfanilamides are wide spectrum drugs effective against Gram ______ bacteria.

a)

+/−

b)

+

c)

−

d)

variable

17.

Fill in the blank: Anti-folates inhibit folic acid biosynthesis by binding to ______.

a)

dihydrofolate reductase

b)

DNA polymerase

c)

RNA polymerase

d)

topoisomerase

18.

What enzyme do sulfa drugs selectively inhibit?

a)

Dihydrofolate reductase (DHFR)

b)

DNA polymerase

c)

RNA polymerase

d)

Peptidoglycan synthase

19.

Why did resistance to sulfa drugs happen fast?

a)

Bacteria can proliferate in ultra low levels of folate

b)

Bacteria are naturally immune

c)

Sulfa drugs are weak

d)

Bacteria mutate quickly

20.

Fill in the blank: Sulfa drugs mimic ______.

a)

PABA

b)

Folic acid

c)

Adenine

d)

Glucose

21.

Trimethoprim binds to DHFR and prevents redox ability to use coenzyme _______.

a)

NADPH

b)

FADH2

c)

ATP

d)

CoA

22.

Which glycopeptide antibiotic is derived from the soil microbe Amycolatopsis from the jungles of Borneo?

a)

Penicillin

b)

Vancomycin

c)

Streptomycin

d)

Erythromycin

23.

Vancomycin attacks which type of bacteria?

a)

Gram negative

b)

Gram positive

c)

Both Gram positive and negative

d)

Fungi

24.

This drug is reserved for treating ________ infections, MRSA, and C.diff.

a)

life-threatening

b)

mild

c)

chronic

d)

viral

25.

Extremely large structure and orally inactive – IV drug. Fill in the blank: This drug is administered as an ________ drug because it is orally inactive due to its extremely large structure.

a)

IV

b)

oral

c)

topical

d)

inhalational

26.

Inhibit biosynthesis of peptidoglycan layer of cell wall. What layer of the cell wall does this drug inhibit the biosynthesis of?

a)

Lipopolysaccharide

b)

Peptidoglycan

c)

Phospholipid

d)

Protein

27.

What does it mean when bacteria are not sensitive to the effects of antibiotics?

a)

It means the bacteria are drug resistant.

b)

It means the bacteria are dead.

c)

It means the bacteria are beneficial.

d)

It means the bacteria are multiplying faster.

28.

Drug resistance in bacteria can be genetically modified by which of the following?

a)

Spontaneous mutations

b)

Overexpression of certain genes

c)

Acquisition of genetic material from other microbes

d)

All of the above

29.

Fill in the blank: Overexpression of certain genes and overproduction of their gene products can lead to ________ in bacteria.

a)

drug resistance

b)

cell lysis

c)

nutrient deficiency

d)

decreased metabolism

30.

Which process involves the exchange of genetic material from other microbes, such as by plasmid DNA exchange?

a)

Acquisition of genetic material

b)

Binary fission

c)

Protein synthesis

d)

Cellular respiration

31.

Resistance can be established by which of the following mechanisms?

a)

Enzyme catalyzed reaction that renders antibiotic inactive

b)

Mutations changing the biological target in the microbe

c)

Up-regulation of drug efflux from the cell

d)

All of the above

32.

Decreased cell wall permeability by mutation of genes can establish drug resistance in bacteria.

a)

True

b)

False

33.

What is the role of biofilm formation in drug resistance?

a)

Biofilm formation resists penetration by antibiotics.

b)

Biofilm formation increases the metabolic rate of bacteria.

c)

Biofilm formation enhances the immune response against bacteria.

d)

Biofilm formation reduces bacterial communication.

34.

Antibiotics that affect cell wall crosslinking

a)

Penicillins

b)

Cephalosporins

c)

Vancomycin

d)

All of the above

e)

None of the above

35.

Antibiotics that target the bacterial ribosome.

a)

Tetracyclines, aminoglycosides, macrolides, chloramphenicol

b)

Penicillins, cephalosporins, carbapenems, monobactams

c)

Quinolones, sulfonamides, trimethoprim, nitrofurantoin

d)

Polymyxins, daptomycin, fosfomycin, bacitracin

36.

Consider the structure shown below. What class of anti-infectious agents does it belong to?

a)

macrolides

b)

Penicillins

c)

vancomycin

d)

fluoroquinolones

e)

Sulfanilamide

37.

Who discovered the tobacco mosaic virus in 1892?

a)

Russian botanist

b)

German chemist

c)

French microbiologist

d)

British physicist

38.

In 1901, which disease did Walter Reed discover was caused by a virus?

a)

Influenza

b)

Yellow fever

c)

Smallpox

d)

Measles

39.

In what year did the electron microscope first show the structure of viruses?

a)

1920

b)

1940

c)

1960

d)

1980

40.

Viruses consist of RNA or DNA, protein, and possibly ________.

a)

carbohydrates

b)

lipids

c)

minerals

d)

vitamins

41.

Do viruses replicate outside of a cell?

a)

True

b)

False

42.

Viruses can contain RNA or DNA (not both), protected by a ______ which is enclosed by a viral envelope covered in glycoproteins.

a)

capsid

b)

ribosome

c)

plasmid

d)

nucleus

43.

Viruses adapt to their environment and mutate and replicate rapidly.

a)

True

b)

False

44.

What is Oseltamivir (Tamiflu) used to treat?

a)

Type A and B influenza

b)

Hepatitis C virus

c)

Bacterial infections

d)

Fungal infections

45.

Oseltamivir (Tamiflu) is recommended for use in the first ___ hours of infection.

a)

48

b)

24

c)

72

d)

12

46.

What is the mechanism of action (MOA) of Oseltamivir (Tamiflu)?

a)

Protease inhibitor

b)

Neuraminidase inhibitor

c)

Reverse transcriptase inhibitor

d)

Polymerase inhibitor

47.

Which of the following is NOT a side effect of Oseltamivir (Tamiflu)?

a)

Cough

b)

Diarrhea

c)

Nausea

d)

Rash

48.

Ribavirin (Virazole) is a broad spectrum antiviral drug discovered in which year?

a)

1970

b)

1965

c)

1982

d)

1978

49.

Ribavirin (Virazole) is a 1st line agent against which virus when combined with interferon-α (INF-α)?

a)

Influenza virus

b)

Hepatitis C virus

c)

Herpes simplex virus

d)

Human immunodeficiency virus

50.

Interferon-α (INF-α) is a natural protein synthesized by immune cells in response to viral infection.

a)

True

b)

False

51.

What is the name of the new ribavirin prodrug that is in Phase III trials and is expected to have fewer side effects?

a)

Ledipasvir

b)

Sofosbuvir

c)

Viramidine

d)

Harvoni

52.

Viramidine is a ________ that diminishes the rate of viral replication. (Fill in the blank)

a)

purine nucleoside analog

b)

protein kinase inhibitor

c)

antibiotic peptide

d)

lipid synthesis blocker

53.

This combo therapy is successful in what percentage of new cases (<6 months)?

a)

50%

b)

70%

c)

90%

d)

100%

54.

What is a side effect of viramidine therapy?

a)

Hypertension

b)

Hemolytic anemia

c)

Diabetes

d)

Renal failure

55.

Ledipasvir & Sofosbuvir (Harvoni) is a 1X daily pill that cures hepatitis C virus in most people in how many weeks?

a)

2-4 weeks

b)

4-6 weeks

c)

8-12 weeks

d)

16-20 weeks

56.

The cure rate for Ledipasvir & Sofosbuvir (Harvoni) is ________%.

a)

94-99

b)

60-70

c)

75-80

d)

85-90

57.

Viruses contain which type of nucleic acids for their genetic material?

a)

ssDNA

b)

dsDNA

c)

ssRNA

d)

dsRNA

58.

Which of the following is the genetic material of HIV?

a)

ssDNA

b)

dsDNA

c)

ssRNA

d)

dsRNA

e)

DNA/RNA hybrid

59.

HIV stands for ________.

a)

human immunodeficiency virus

b)

human infectious virus

c)

highly infectious virus

d)

human immune vaccine

60.

HIV attacks and gradually destroys the immune system leading to ________ (AIDS).

a)

acquired immunodeficiency syndrome

b)

acute immune disorder syndrome

c)

autoimmune deficiency system

d)

advanced infection disease syndrome

61.

Approximately how many people get infected with HIV in the US each year?

a)

~50,000

b)

~5,000

c)

~500,000

d)

~500

62.

HIV uses ________ to convert ssRNA to ssDNA to dsDNA.

a)

reverse transcriptase

b)

DNA polymerase

c)

RNA polymerase

d)

ligase

63.

Which of the following is a class of drugs used in HIV treatment?

a)

Reverse transcriptase inhibitor

b)

Beta-blocker

c)

Antifungal

d)

Antihistamine

64.

What is the mechanism of action of CCR5 receptor antagonists?

a)

HIV entry inhibitor

b)

DNA synthesis inhibitor

c)

Protein synthesis inhibitor

d)

Cell wall synthesis inhibitor

65.

Zidovudine (Retrovir, AZT) was originally synthesized as an anti-cancer agent in which year?

a)

1964

b)

1972

c)

1981

d)

1957

66.

AZT is converted to 5-triphosphate thymidine derivative that is incorporated into DNA by reverse transcriptase causing ________.

a)

termination

b)

elongation

c)

mutation

d)

replication

67.

At high doses, Zidovudine (AZT) has severe side effects such as bone marrow toxicity, anemia, and ________.

a)

neutropenia

b)

hepatitis

c)

hyperglycemia

d)

alopecia

68.

Which drug is a deoxycytidine derivative with a similar mechanism to Zidovudine?

a)

Zalcitabine

b)

Lamivudine

c)

Tenofovir

d)

Abacavir

69.

Which of the following drugs are used together as an HIV protease inhibitor combo only?

a)

Lopinavir + Ritonavir

b)

Zidovudine + Lamivudine

c)

Efavirenz + Tenofovir

d)

Abacavir + Dolutegravir

70.

Lopinavir and Ritonavir are ________ of the reaction catalyzed by HIV protease.

a)

transition state analogs

b)

substrates

c)

cofactors

d)

competitive inhibitors

71.

The effect of combining Lopinavir and Ritonavir on the half-life of Lopinavir is:

a)

It increases the half-life of Lopinavir.

b)

It decreases the half-life of Lopinavir.

c)

It has no effect on the half-life of Lopinavir.

d)

It causes unpredictable changes in the half-life of Lopinavir.

72.

What is the main action of Selzentry (Maraviroc) in HIV treatment?

a)

Blocks attachment of HIV to CCR5 surface receptors of T-cells

b)

Inhibits reverse transcriptase

c)

Blocks CXCR4 receptor

d)

Inhibits protease

73.

Selzentry (Maraviroc) is effective in blocking the CXCR4 receptor.

a)

True

b)

False

74.

List two severe side effects that Selzentry (Maraviroc) can cause.

a)

Severe liver symptoms, severe skin and hypersensitivity reactions, and cardiovascular events.

b)

Mild headache and runny nose.

c)

Drowsiness and increased appetite.

d)

Dry mouth and constipation.

75.

Which of the following is NOT a component of the combination drug Biktarvy?

a)

A) Bictegravir

b)

B) Emtricitabine

c)

C) Tenofovir alafenamide

d)

D) Maraviroc

76.

Bictegravir, a component of Biktarvy, is classified as a(n) ______ inhibitor.

a)

integrase

b)

protease

c)

reverse transcriptase

d)

fusion

77.

Emtricitabine, found in Biktarvy, is a ______ reverse transcriptase inhibitor.

a)

nucleoside

b)

non-nucleoside

c)

protease

d)

integrase

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