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PHAC 3001 > Midterm #3 > Flashcards

Midterm #3 Flashcards

1
Q

Penicillin Drugs

A
  • penicillin (G and V)

- amoxycillin

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2
Q

Beta Lactam Drugs

A
  • Cephalosporin

- Carbapenems

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3
Q

Cell Wall Attacking Drugs

A
  • Vancomycin

- Bacitracin

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4
Q

3 classes of drugs that attack cell wall

A
  • penicillin
  • beta lactam drugs
  • other cell well inhibitors (not penicillin based)
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5
Q

Penicillin

A

Mechanism - enters the cell, binds to PBP to inhibit it’s role in strengthening the peptidoglycan layer. Cell lysis.

  • penicillin G breaks down in acid
  • amoxycillin has a longer half life, has an effect o gram -‘ve bacteria, and has higher bioavailability. Better version of penicillin.
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6
Q

What effects the activity of penicillin?

A

porins - improve effect

beta lactamase - inhibit effect

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7
Q

Beta lactamase inhibitor

A

clavulanate

mechanism - occupies beta lactamase

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8
Q

Cephalosporins

A

structure next to the beta lactamase ring is slightly different than penicillin. Makes it more resistant to beta lactamase.

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9
Q

Carbapenems

A
  • S in penicillin is changed to C in carbapenems - makes it beta lactamase resistant.
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10
Q

Vancomycin

A

inhibits growth/elongation of peptidoglycan strands. Unable to make a rigid structure without long strands. Lysis.

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11
Q

Bacitracin

A

works inside the cell (not at the location of the cell wal)) to inhibit cell wall formation

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12
Q

Classes of Drugs that inhibit protein synthesis (effect ribosomal subunits)

A
  • Chloramphenicol
  • Erythromycin
  • Aminoglycosides
  • Tetracyclines
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13
Q

Chloramphenical

A

binds to the 50S sunubit. Inhibits formation of peptide bonds between individual amino acids
- side effects - bone marrow disturbance, gray baby syndrome, serious drug interactions.

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14
Q

Erythromycin

A

changes the 30S subunit, causing the mRNA code to be read incorrectly (wrong amino acid)

  • unstable in acid
  • a macrolide
  • used if a penicillin resistance develops.
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15
Q

Macrolide Drugs

A

Erythromycin < Clarithromycin < Azithromycin

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16
Q

Clarithromycin

A

same effect as erythromycin but can be given orally

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17
Q

Azithromycin

A

some effect on gram -‘ve
more potent
greater tissue penetration.
- better drug

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18
Q

Aminoglycosides

A

bind 50S subunit - prevents ribosomal movement along mRNA.

  • streptomycin, gentamicin
  • hexose ring linked to an amino sugar by a glycosidic linkage.
  • effective against gram -‘ve
  • given via IV
  • side effects - ototoxic, nephrotoxic.
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19
Q

Aminoglycoside Mechanism (3)

A
  • mRNA binds 30S, but 50S doesn’t join.
  • miscoding in the polypeptide chain - causes the tRNA to hold the wrong amino acid
  • blocks translocation
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20
Q

Tetracyclines

A

interfere with the acceptor site

  • absorption effected by milk and antacids
  • accumulates in bones and teeth.
  • shouldn’t be given to pregnant woman or children.
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21
Q

Drugs that inhibit DNA Synthesis

A

sulfonamides

trimethoprim

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22
Q

Folic acid pathway

A

PABA -(DHPS)-> folate -(DHFR)-> THF -> Purines for DNA

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23
Q

Sulfonamide

A

Target and inhibit DHPS

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24
Q

Trimethoprims

A

Target and inhibit bacterial DHFR (because DHFR is in human cells too)

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25
Q

Other DHFR inhibitors

A

protozoa - pyrimathamine

cancer - methotrexate

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26
Q

DNA Replication inhibiting Drugs

A

Fluoroquinolones = fluorinated quinolones = ciprofloxacin

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27
Q

Activity of Fluoroquinolones

A

inhibit DNA gyrase/bacterial topoisomerase activity. DNA can’t be uncoiled so it can’t be replicated.

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28
Q

Problem with fluoroquinolones?

A

widespread resistance

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29
Q

Cell Membrane inhibiting Drugs

A

Polymyxins

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30
Q

Polymyxins

A
  • detergent-like properties.

- destroy phospholipid membrane by binding to PE in the membrane and cause disruption to the structure.

31
Q

Problem with polymyxins?

A

also has the same effect on human cells.

- can only be given topically. Never systemically

32
Q

Common Combination Therapies

A
  • chloramphenicol + aminoglycosides
  • beta-lactam drugs + beta lactam inhibitors
  • 2 beta lactam drugs that inhibit different PBPs
  • sulfonamides and trimethoprims
33
Q

Advantages of Combination Therapy

A
  • wider spectrum
  • can give lower doses
  • synergism
34
Q

Disadvantages of Combination Therapy

A
  • antagonism
  • adverse effects
  • increased likelihood of resistance
35
Q

Bacterial Resistance

A
  • decreased entry
  • efflux pump
  • bypass pathway
  • altered target proteins
  • enzymes to degrade the drug
36
Q

Examples of Bacterial Resistance

A

Sulfonamide resistance

Trimethoprim resistance

37
Q

Sulfonamide Resistance

A
  • decrease membrane permeability
  • increased PABA
  • change DHPS so it nolonger binds to sulfonamide
38
Q

Trimethoprim Resistance

A
  • decrease membrane permeability
  • increase DHFR
  • change DHFR so it not longer binds to trimethoprim.
39
Q

Drugs for Fungi

A
  • ketoconazole - oral
  • fluconazole - oral
  • amphotericin B - IV
40
Q

Fluconazole

A

inhibits fungal cytochrome P450 -> enzyme involved in making ergosterone

41
Q

Amphotericin B

A

amphoteric - one end is hydrophilic and the other is hydrophobic. Therefore it happily spans the membrane.
makes pores by binding to ergosterol.
- sometimes binds to cholesterol in humans - super dangerous - nephrotoxicity.

42
Q

Causes of Cancer

A

Genetics
- oncogenes
- tumor suppressor genes
Environment - most important

43
Q

Cancer Pathophysiology

A

1) Initiation - 1 cell gets mutated
2) Promotion - proliferation
3) Progression - malignant.

44
Q

3 ways we treat cancer

A

1) surgery
2) radiation
3) chemotherapy

45
Q

Traditional Cancer Treatments

A

Alkylating & Platinum Agents - target the DNA molecule itself.
Antimetabolites - target DNA synthesis
Antobiotics and Topoisomerase inhibitors - target transcription
Vinca Alkaloids & Taxanes - target the mitotic spindle.

46
Q

Alkylating & Platinum Agents

A

alkylating - cyclophosphamide
platinum - cisplatin
mechanism - both bind the DNA strand, are detected as damage and cause DNA molecule death.
Cl is removed and 2 (incorrect) DNA base pairs covalently bind - destroyed.
Negative side effects - can also bind to other similar structures like lipids ad proteins - problematic for other bodily cells.

47
Q

Antimetabolites

A

Purine antagonists - mercaptopurine
Pyrimidine antagonists - fluorouracil
Folic Acid antagonists - methotrexate
cell cycle specific - S phase drugs.

48
Q

Mercaptopurine

A
  • looks like adenine.
  • inserts itself where adenine would bind in DNA and RNA.
  • DNA enzymes recognize that DNA is wrong and destroy it.
49
Q

Fluorouracil

A
  • looks like U/T
  • binds to thymidylate synthase, preventing thymidine form being made.
  • can’t make any new DNA
50
Q

Methotrexate

A
  • inhibits cancer cell specific DHFR

- unable to make new nucleotides.

51
Q

Antibiotic & Topoisomerase Inhibitors

A

Topoisomerase I inhibitors - topotecan
Topoisomerase II inhibitors - doxorubicin
Antibiotics - anthracycline

52
Q

Topotecan

A

binds topoisomerase I, produces a fixed complex, inhibits DNA unwinding.
- leads to cell death

53
Q

Doxorubicin

A

Binds topoisomerase II, prevents religation of DNA

- leads to cell death

54
Q

Anthracycline

A

wedges itself between DNA, stabilized topoisomerase II complex, preventing religation.

  • produces free radical
  • unique cardiotoxicity
55
Q

Vinca Alkaloids & Taxanes

A

Vinca Alkaloid - vincristine

Taxane - docetaxel

56
Q

Vincristine

A

blocks assembly of microtubules in mitotic spindle.

57
Q

Docataxel

A

blocks disassembly of microtubules in mitotic spindle.

58
Q

Adverse effects of Traditional Antineoplastics?

A
  • non-specific
  • small therapeutic window
  • immuno-suppressant
59
Q

Combination Drugs

A
  • must be effective by themselves
  • should have similar recovery intervals/rates
  • pick drugs with different aide effects so not to be additive.
60
Q

Combination Therapy Example

A

CAV for lung cancer
C - cyclophosphamide
A - adriamycin (brand name for doxorubicin
V - vincristine

61
Q

Targeted Anticancer Drugs - 5 targets

A

1) Cellular Markers
2) New Blood Vessel Growth - angiogenesis
3) Growth and Proliferation
4) Survival Proteins
5) Hormone Sensitive Cancer

62
Q

Cellular Markers

A

CD-20 is a common cancer cell marker
also found on mature B cells
- monoclonal antibody - flags for immune system.
- conjugated radiation - kills cells with radiation that antibody binds to.
- conjugated cytotoxicity - kills cells through antimicrotubule action (eg. vincristine)

63
Q

Tositumomab

A

radiation conjugated, monoclonal antibody targeted to CD-20.

64
Q

Sipuleucel-T

A

anti-cancer vaccine.

virus expressing CD-20, activates immune system to respond to cells presenting CD-20

65
Q

Bevacizumab

A

monoclonal antibody against VEGF.

  • similar to VEGF, binds the VEGFR to inhibit binding and downstream signaling.
  • inhibit angiogenosis
66
Q

Sorafenib & Gefitinib

A

Small molecule TK inhibitor. Binds intracellular part of the tyrosine kinase to inhibit autophosphorylation and activation

  • specific to receptor tyrosine kinases like HER-2
  • inhibit angiogenesis
67
Q

Trastuzumab

A

blocks EGF receptors.

  • EGF - epidermal growht factors stimulates growth and proliferation of cancer cells.
  • can be conjugated (cytotoxic) or unconjugated (just antagonistic)
  • inhibits growth and proliferation
68
Q

Imatinib

A

Bcl-2 is a survival protein that allows cells to ignore the apoptosis signal.
Bcl-Abl is a cytoplasmic TK involved in Bcl-2 upregulation.
Imatinib binds to Bcl-Abl, so the normal ligand can not bind/activate it. (anagonist)
- inhibits survival proteins

69
Q

Hormone Sensitive Cancer Drugs

A
  • Leuprolide
  • Letrozole
  • Tamoxifen
70
Q

Leuprolide

A

looks like GnRH, involved in the production of testesterone and estrogen.
- effective against both breast cancer and prostate cancer

71
Q

Letrozole

A

inhibits aromatase involved in estrogen conversion

- specific to breast cancer

72
Q

Tamoxifen

A

estrogen receptor antagonist

- specific to breast cancer

73
Q

1st line therapy

A 
Old + New
Eg. R-CHOP
R - rituximab
C - cyclophosphamide 
H - hydroxydaunorubicin (doxorubicin)
O - oncovin (vincrisitne)
P - prendisone adjuvant (reduce side effects)

PHAC 3001 (1 decks)

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