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Med Chem modules > Chemotherapy > Flashcards

Chemotherapy Flashcards

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1
Q

Why do microbes require a cell wall?

A

Prevents unlimited swelling that would occur due to high osmotic pressure

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2
Q

List 5 features of prokaryotes distinct from eukaryotes that represent exploitable differences

A 
Cell wall
Nucleic acid synthesis 
Protein synthesis 
The cell membrane
Respiratory election transport chain
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3
Q

What are bacteriocidal antibiotics?

A

Kill bacteria

Do not require a competent immune system

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4
Q

Describe gram negative bacteria.

A

Doesn’t stain with violet gram stain
Thin wall
Complex lipopolysaccharide/proteoglycan wall
More resistant to antibiotics due to compex wall

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5
Q

What is the mycobacteria cell wall features?

A

Composed of mycolic acid

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6
Q

What are bacteriostatic drugs?

A

Slow bacterial proliferation
Reduced the ability for microbes to divide
Require a competent immune system to work

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7
Q

What is the fungi cell wall features?

A

Uses ergosterol instead of cholesterol as primary sterol

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8
Q

What are the glycopeptide components of the proteoglycan cell wall

A

N-acetyl-glucosamide

N-acetyl-muramate

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9
Q

What is the enzyme responsible for cross-linking the polymers?

A

Transpeptidase

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10
Q

What specific amino acid dipeptide is bound and cleaved by transpeptidase?

A

D-analyl-D-alanine

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11
Q

Why won’t beta-lactam antibiotics affect human alanine cross links?

A

Human alanine is L-alanine
Human transpeptidase will not recognise and bind to beta-lactams as the receptor site will be stereospecific for L-alanine.

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12
Q

What are the beta-lactams?

A

Penicillins
Cephalosporins
Carbepanems

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13
Q

What does the beta-lactam ring mimic? What is its affect?

A

Mimic the D-alanyl-D-alanine peptide bonds

It’s inhibits transpeptidase

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14
Q

How do the beta-lactamase enzymes eliminate the effectiveness of the beta lactams?

A

It hydrolysises the amide bond of the beta lactam ring. This causes ring opening, deactivating the antibiotic

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15
Q

What limited the bioavailability of penicillin? How was this addressed?

A

Beta-lactamases eliminated the effectives of penicillin

Semi-synthetic penicillins resistant to beta-lactamases were produced

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16
Q

What improvements have been made to penicillins?

A

Gastric acid resistance

Wider range/specificity to different strains

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17
Q

With a beta-lactamase sensitive penicillin, what adjuncts can be used to increase bioavailability?

A

Clavulanic acid

Inhibits beta-lactamase

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18
Q

If infected with MRSA, what antibiotic is used? What’s the mechanism?

A

Vancomycin:

Inhibits proteoglycan wall synthesis by high affinity binding to precursors preventing transglycosylation

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19
Q

Describe gram positive bacteria

A

Stain with violet gram stain
Thick wall
Simple peptidoglycan wall

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20
Q

What do polymixins do?

A

Interact with phospholipids (loosening the wall) of the cell wall, destroying the selective barrier function, so the bacteria is flooded with unwanted ions

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21
Q

Name a penicillin resistant to beta-lactamase activity

A

Flucloxacillin

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22
Q

Are polymixins more effective against gram negative or positive bacteria?

A

Gram negative

They’re selective for lipopolysaccharides

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23
Q

Why are polymixins limited to topical use?

A

They’re not absorbed by the GI tract

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24
Q

List antibiotics used to treat tuberculosis and leprosy

A

Isoniazid

Ethambutol

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25
Q

What part of the folic acid molecule do sulphonamides mimic?

A

The pABA region

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26
Q

What mimics the pteridine part of the folic acid molecule?

A

Trimethoprim

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27
Q

What do sulphonamides do?

A

Inhibit dihydropteroate synthase, preventing the conversion of pABA to folate

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28
Q

What does trimethoprim do?

A

Inhibits dihydrofolate reductase preventing the conversion of folate to tetrahydrofolate

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29
Q

Which sulfonamide derivative has activity against mycobacteria?

A

Sulfones

30
Q

What do quinolones do?

A

Bacteriocidal

They inhibit DNA topoisomerase II

31
Q

What does rifamycin do?

A

They’re macrocyclic antibiotics
Targets mycobacteria causing leprosy and tuberculosis
Inhibits DNA polymerase

32
Q

What’s the difference between eukaryotic and prokaryotic ribosome structures?

A

Eukaryotic are denser, having 40S and 60S subunits

Prokaryotic ribosomes have 30S and 50S

33
Q

What do tetracyclines do?

A

Affect aminoacyl tRNA binding

34
Q

What do aminoglycosides do?

A

They affect the recognition of aminoacyl tRNA/mRNA to codon/anticodon

35
Q

What antibiotic affects transpeptidation in protein synthesis?

A

Chloramphenicol

36
Q

What causes peptidyltranslocation?

A

Macrolides

37
Q

How do 5-nitroimadazoles operate to eliminate anaerobic bacteria?

A

If oxygen is not terminal acceptor, the electron transport chain (ETC) is at a lower potential
They’re terminal acceptors at a sufficiently low potential
Ferrodoxin in the ETC transports 2 electrons to 5-nitroimadazoles
Reduction converts drug to a cross linker which disrupts DNA integrity
ETC in humans at a potential too high

38
Q

What drug inhibits ergosterol synthesis

A

Imadazole/triazole

39
Q

What drug permeates fungal membrane by interacting with ergosterol?

A

Polyene

40
Q

What drug inhibits fungal mitosis?

A

Griseofulvin:

Binds to tibulin, interfering with microtubule function

41
Q

Give the 4 exploitable stages of the viral life cycle

A

Attachment and entry
Viral nucleic acid replication
Production of viral proteins, coat assembly of virions
Viral relaease, shedding and egress

42
Q

How can you target viral entry?

A

Interfering with how they interact with host cell receptors

Pinocytosis

43
Q

Whats a positive virus?

A

Their genes can be directly accessed by host ribosomes

44
Q

What’s a negative virus?

A

Genes cannot be directly accessed by host ribosomes

45
Q

What’s a retrovirus?

A

Virus has RNA which is coverts to DNA which is then processed

46
Q

What are the 4 types of virus?

A

Positive
Negative
Retro
DNA

47
Q

What drug actually like amantadine?

A

Rimantidine

48
Q

How does amantadine work?

A

Binds to viral coded H channel (M2) to prevent endosome acidification
Since pH is not low enough, the viral membrane cannot fuse with the endosome membrane
The virus cannot enter the cell

49
Q

What is the more accurate name of reverse transcriptase?

A

RNA dependent DNA polymerase

50
Q

Why are nucleoside rather than nucleotide analogues used as drugs?

A

Nucleosides can cross the cell membrane

Nucleotides are too charged

51
Q

Name 2 nucleoside inhibitors of reverse transcriptase used for HIV.

A

AZT ddC

52
Q

What feature of nucleoside inhibitors suppress viral nucleic acid synthesis?

A

DNA chain termination

53
Q

Name a non-nucleoside reverse transcriptase inhibitor

A

C1-TIBO

54
Q

Name a HIV protease inhibitor

A

Indinavir

55
Q

Why do protease inhibitors represent an exploitable difference?

A

Viral proteins are polycistronic
They require a viral protease to cleave the propeptide into structural proteins
Inhibiting the viral protease prevents the formation of the structural proteins

56
Q

What is HAART?

A

High activity antiretroviral therapy
Decreases the mutation probability conferring mutatation
NRTIs, NNRTIs, protease inhibitors are used in combo. And sub. max. doses to reduce toxicity

57
Q

Name a drug that selectively affects infected cells. How does it work?

A

Aciclovir:

Selectively phosphorylated by viral thymidine kinase

58
Q

What does foscarnet do?

A

Treats cytomegalovirus

59
Q

What’s the mechanism of action of ribavarin?

A

Inhibits RNA polymerase

Inhibits GTP dependent enzymes (affects viral mRNA capping)

60
Q

What are endogenous antiviral agents?

A

Interferons

61
Q

What do interferons do?

A

Inhibit the entry of viruses
Induce latent RNAase (degrades viral mRNA)
Suspension of ribosome function by phosphorylation and inhibition of eIF2

62
Q

Name 2 neuraminidase inhibitors

A

Osaltamivir

Zanamivir

63
Q

How does enfurviratide work?

A

Causes the fusion of HIV I a macrophage membrane and then entry into the macrophage

64
Q

Name the four main classes of anti cancer drugs

A

Alkylating agents
Antimetabolites
Cytotoxic antibodies
Plant derivatives

65
Q

How do nitrogen mustards, nitrosureas, and cisplatins operate to inhibit cell proliferation?

A

Cross link guanine nucleotides in DNA so DNA cannot be replicated or transcribed

66
Q

What stage of cell cycle donitrogen mustards, nitrosureas, and cisplatins target?

A

S phase

67
Q

Describe a cytotoxic antibody

A

Doxorubicin:

Inhibits the synthesis of nucleic acids in cancer therapy

68
Q

Describe a plant alkaloid

A

Etoposide:

Inhibits the synthesis of nucleic acids in cancer therapy

69
Q

Describe an antimetabolite.

A

Melbotrexate:

Inhibits the synthesis of nucleic acids in cancer therapy

70
Q

Name 3 cytotoxic drugs that inhibit polymerase activity

A

Dactinomycin
Doxorubicin
Etoposide

71
Q

What cell phase do vinca alkaloids and toxanes target?

A

M Phase

72
Q

What anti cancers prevent microtubule polymerisation, hence mitosis?

A

Vinca alkaloids and toxanes

Med Chem modules (8 decks)

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