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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
Other DHFR inhibitors
protozoa - pyrimathamine | cancer - methotrexate
26
DNA Replication inhibiting Drugs
Fluoroquinolones = fluorinated quinolones = ciprofloxacin
27
Activity of Fluoroquinolones
inhibit DNA gyrase/bacterial topoisomerase activity. DNA can't be uncoiled so it can't be replicated.
28
Problem with fluoroquinolones?
widespread resistance
29
Cell Membrane inhibiting Drugs
Polymyxins
30
Polymyxins
- detergent-like properties. | - destroy phospholipid membrane by binding to PE in the membrane and cause disruption to the structure.
31
Problem with polymyxins?
also has the same effect on human cells. | - can only be given topically. Never systemically
32
Common Combination Therapies
- chloramphenicol + aminoglycosides - beta-lactam drugs + beta lactam inhibitors - 2 beta lactam drugs that inhibit different PBPs - sulfonamides and trimethoprims
33
Advantages of Combination Therapy
- wider spectrum - can give lower doses - synergism
34
Disadvantages of Combination Therapy
- antagonism - adverse effects - increased likelihood of resistance
35
Bacterial Resistance
- decreased entry - efflux pump - bypass pathway - altered target proteins - enzymes to degrade the drug
36
Examples of Bacterial Resistance
Sulfonamide resistance | Trimethoprim resistance
37
Sulfonamide Resistance
- decrease membrane permeability - increased PABA - change DHPS so it nolonger binds to sulfonamide
38
Trimethoprim Resistance
- decrease membrane permeability - increase DHFR - change DHFR so it not longer binds to trimethoprim.
39
Drugs for Fungi
- ketoconazole - oral - fluconazole - oral - amphotericin B - IV
40
Fluconazole
inhibits fungal cytochrome P450 -> enzyme involved in making ergosterone
41
Amphotericin B
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
Causes of Cancer
Genetics - oncogenes - tumor suppressor genes Environment - most important
43
Cancer Pathophysiology
1) Initiation - 1 cell gets mutated 2) Promotion - proliferation 3) Progression - malignant.
44
3 ways we treat cancer
1) surgery 2) radiation 3) chemotherapy
45
Traditional Cancer Treatments
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
Alkylating & Platinum Agents
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
Antimetabolites
Purine antagonists - mercaptopurine Pyrimidine antagonists - fluorouracil Folic Acid antagonists - methotrexate cell cycle specific - S phase drugs.
48
Mercaptopurine
- looks like adenine. - inserts itself where adenine would bind in DNA and RNA. - DNA enzymes recognize that DNA is wrong and destroy it.
49
Fluorouracil
- looks like U/T - binds to thymidylate synthase, preventing thymidine form being made. - can't make any new DNA
50
Methotrexate
- inhibits cancer cell specific DHFR | - unable to make new nucleotides.
51
Antibiotic & Topoisomerase Inhibitors
Topoisomerase I inhibitors - topotecan Topoisomerase II inhibitors - doxorubicin Antibiotics - anthracycline
52
Topotecan
binds topoisomerase I, produces a fixed complex, inhibits DNA unwinding. - leads to cell death
53
Doxorubicin
Binds topoisomerase II, prevents religation of DNA | - leads to cell death
54
Anthracycline
wedges itself between DNA, stabilized topoisomerase II complex, preventing religation. - produces free radical - unique cardiotoxicity
55
Vinca Alkaloids & Taxanes
Vinca Alkaloid - vincristine | Taxane - docetaxel
56
Vincristine
blocks assembly of microtubules in mitotic spindle.
57
Docataxel
blocks disassembly of microtubules in mitotic spindle.
58
Adverse effects of Traditional Antineoplastics?
- non-specific - small therapeutic window - immuno-suppressant
59
Combination Drugs
- must be effective by themselves - should have similar recovery intervals/rates - pick drugs with different aide effects so not to be additive.
60
Combination Therapy Example
CAV for lung cancer C - cyclophosphamide A - adriamycin (brand name for doxorubicin V - vincristine
61
Targeted Anticancer Drugs - 5 targets
1) Cellular Markers 2) New Blood Vessel Growth - angiogenesis 3) Growth and Proliferation 4) Survival Proteins 5) Hormone Sensitive Cancer
62
Cellular Markers
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
Tositumomab
radiation conjugated, monoclonal antibody targeted to CD-20.
64
Sipuleucel-T
anti-cancer vaccine. | virus expressing CD-20, activates immune system to respond to cells presenting CD-20
65
Bevacizumab
monoclonal antibody against VEGF. - similar to VEGF, binds the VEGFR to inhibit binding and downstream signaling. - inhibit angiogenosis
66
Sorafenib & Gefitinib
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
Trastuzumab
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
Imatinib
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
Hormone Sensitive Cancer Drugs
- Leuprolide - Letrozole - Tamoxifen
70
Leuprolide
looks like GnRH, involved in the production of testesterone and estrogen. - effective against both breast cancer and prostate cancer
71
Letrozole
inhibits aromatase involved in estrogen conversion | - specific to breast cancer
72
Tamoxifen
estrogen receptor antagonist | - specific to breast cancer
73
1st line therapy
``` 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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