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CPPS 304 > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

What is chemotherapy?

A

Use of drugs(chemicals) to eradiate pathogenic organisms or neoplastic cells in the treatment of infectious diseases or cancer.

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2
Q

What is selective toxicity?

A

A chemotherapeutic drug inhibits a vetal finction of invading organisms or neoplatic cells that differs from host cells.

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3
Q

What classes do chemotherapeutic drugs include?

A
  • Antimicrobial drugs (Antimicrobacterial, antifungal, antiviral)
  • Antiparasitic Drugs
  • Antineoplastic and Immunopharmacology Drugs
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4
Q

What are antimicrobial drugs classified based off of?

A

Basd on their site and mechanism of action and are subclassified on the basis of their chemical structure.

  • Cell wall synthesis inhibitors
  • protein sythesis inhibitors
  • metabolic and. nucleic acid inhibitors
  • cell membrane inhibitors
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5
Q

What does antimicrobial activity of a drug is influenced based on what?

A
  • The drugs bactericidal or bacteriostatic effect
  • The spectrum of activity against important groups of pathogens.
  • Its concentration and time dependant effects on sensitive organisms.
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6
Q

What does bacteriocidal and bacteriastatic mean?

A

Bactericidal Drug: Kills Sensitive Organisms so that the number of viable organisms falls rapidly after exposure to the drug. (Induce lethal changes in metabolism or block essential activityes for viable organisms.)

Bacteriostatic: Inhibits the growth of bacteria but does not kill them. - Bacteria remain relatively constant. (Inhibit a metabolic reaction needed for growth not survuval)

Same principles for fungicidal and fungistatic.

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7
Q

What are some examples of bactericidal and bacteriostatic drugs?

A

**Bactericidal **

  • Penicillins - Inhibit sythesis of Cell Wall
  • Streptomycin - Irreversibly inhibits protein synthesis.

Bacteriostatic

  • Sulfonamides - Block synthesis of Folic Acid
  • Tetracyclines - Reversibly Inhibit Protein Synthesis

Erythromycin - Can be either depending on concentration and traget species.

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8
Q

What are the 3 types of spectrum of Antimicrobial Drugs?

A
  • Narrow-Spectrum
  • Extended-Spectrum
  • Broad-Spectrum
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9
Q

What is the MIC, CDKR, and PAE?

A

Minimal Inhibitory Concentration (MIC) - the lowest cocentration of a drug that inhibits bacterial growth. Based on the MIC, a particular strain of bacteria can be classified as susceptible or resistance to a particular drug.

Concentration-Dependant Killing Rate (CDKR)

The Post Antibiotic Effect (PAE)

Penicillins and Macrolide - Show PAE against gram positive Cocci Aminoglycosides - Have CDKR and PAE (against gram negative bacilli) - Entire dose can be given at one time -> Make sure all bacteria are killed and stay like that.
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10
Q

What are 3 laboratory tests to test Microbial Sensitivity?

A
  • Broth Dilution Test
  • Disk Diffusion Method (Kirby-Bauer Test)
  • E-test Method
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11
Q

What is the Broth Dilution Test?

A
1ug/ml
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12
Q

What is the Disk Diffusion (Kirby-Bauer) Method?

A
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13
Q

What is the E-Test Method?

A
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14
Q

Organism can be classified as suseptibal,intermidiate, resistant to drug

What is these categories based on?

A

The realtionship between the MIC and the Peak Serum Concentration.

**MIC (Minimum Inhibitory Concentration):
**
The lowest concentration of a drug that inhibits visible growth of a pathogen.
Lower MIC means the drug is more effective against the pathogen.

Peak Serum Concentration:

The highest concentration of the drug in the bloodstream after administration of a typical dose.

The peak serum concentration of a drug should be 4
to 10 times greater than the MIC for a pathogen to be
susceptible to a drug.
24

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15
Q

What are the two types of resistance to drugs that microbes have?

A
  • Innate
  • Acquired
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16
Q

What does aquire drug resistance arise from?

A
  • Sponaneous Mutation - Microbes can spontaneously mutate to form resistant to a
    particular antimicrobial drug at a relatively constant rate, such as in 1 in 1012 organisms per unit of time
  • Transfer of Plasmids
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17
Q

What does transferable resistance result from?

Expain in regards to conjugation, transformation, transduction.

A
  • Transferable resistance usually results from bacterial conjugation and the transfer of plasmids (extrachromosomal DNA) that confer drug resistance.
  • Transferable resistance, however, can also be mediated by transformation (uptake of naked DNA) or transduction (transfer of bacterial DNA by a bacteriophage).
  • Bacterial conjugation enables a bacterium to donate a plasmid containing genes that encode proteins responsible for resistance to an antibiotic. These genes are called resistance factors (R factors). The resistance factors can be transferred both within a particular species and between different species, so they often confer multidrug resistance.
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18
Q

u

What are the Primary Mechanisms of Microbial Resistance?

A
  • Inactivation of the drug by microbial enzymes
  • Decreased accumulation of the drug by the microbe.
  • Reduced affinity of the target macromolecule for the drug.
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19
Q

What is P-Glycoprotein?

A

Transports antineoplastic drugs out of human cancer cells.

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20
Q

What is the selection of antimicrobial drugs based on?

A
  • The cause, location, and severity of an infection
  • The age, physiologic status, and immune competency of the patient.
  • The pharmacologic properties of antimicrobial drugs.
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21
Q

What are host factor you should consider when choosing a drug?

A
  • Pregnancy
  • drug allergies
  • age and immune status
  • the presence of renal impairment
  • the presence of hepatic insufficiency
  • the presence of abscesses
  • the presence of indwelling catheters and similar devices
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22
Q

What is Empiric Therapy?

A

Used to treat serious inections until test results are available or to treat minor upper respiratory and urinary tract infections because of the predictability of causative organisms and their sensitivity to drugs.

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23
Q

What are pharmacokinetic properties that influence antibiotic seletion?

A
  • Oral bioavailability
  • peak serum concentration
  • Distribution to particulat sites of infection, routes of elimination, elimination half life.

An ideal antimicrobial drug for ambulatory patients would havegood oral bioavailability and a long plasma half-life so that itwould need to be taken only once a day. Azithromycin is an example of an antibiotic that meets these criteria

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24
Q

Why should the peak serum concentration of an antimicrobial drug be several times greater than the MIC of the pathogenic organism for the drug to eliminate the organism?

A
  • The tissue concentrations of a drug are sometimes lower than the plasma concentration.
  • The urine concentration of an antimicrobial drug can be 10 to 50 times the peak serum concentration. For this reason, infections of the urinary tract can be easier to treat than are infections at other sites.
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25
Q

What bodily sites are not readily penetrated by many antimicrobial drugs?

A

CNS, Bone, Prostate Gland, Ocular Tissues

26
Q

Meningitis needs drugs that achieves good [Conc] in cerebrospinal fluid.

How could you treat meningitis.

A

Penicillin G - Can Penetrate Fluid Barrier
Aminoglycosides - Intrathecal Injection - Does not Penetrate

27
Q

Antimicrobial drug [conc] are low in bone,

How long to Patients with Osteomyelitis need to be treated?

A

Antibiotics for several weeks to produce a cure.

28
Q

How does the prostrate restrict entry of some antimicrobial drugs?

A

Drugs have difficulty crossing the prostatic epithelium due to prostatic fluid having a low pH.

Favor Entry of Weak Bases - Trimethoprim

Excludes Entry of Weak Acids - Penicillin

29
Q

What drugs are effective for treating urinary tract infections?

A

Drugs elimated by Renal Excretion - Flouroquinolones

Better then drugs that get metobolized or biliary excretion.

30
Q

What happens to antibiotics that are usually eliminated in the kidneys in someone whos renal funtion is declined?

A

Can accumulate in patients - Dosage must be reduced.

Aminoglycosides

31
Q

What are the level adverse effects of different antimicrobial drugs?

B-Lactam, Aminoglycosides. Flroroquinones, Tetracyclines.

A

B-Lactam(Penicillins, Cephalosporins) and Macrolide (Erythromycin) - Low Adverse Effects

Aminoglycosides (Gentamicin) - High Adverse Effects

Flouroquinones and Tetracyclines - Intermediate

32
Q

What is Drug combination therapy used to treat?

A
  • Mixed Infections - Caused by more than 1 Pathogen (intra-abdominal infections)
  • Life Threatening Infections - Nosocomial Pneumonia
33
Q

What are the different types of combined effects of drugs?

A
  • Antagonistic: combined effect < effect of either drug alone.
  • Additive: combined effect = sum of independant effects
  • Synergistic: combined effect > sum of independant effects
  • Indifferent: combined = similar to greatest effect produced by either drug alone.
34
Q

Can bactericidal drugs effect be reduced if in presence of a bacteriostatic drug?

A

Yes

Bactericidal drugs are usually more effective against
rapidly dividing bacteria, and their effect may be
reduced if bacterial growth is slowed by a bacteriostatic
drug (e.g., chloramphenicol or tetracycline).
44

35
Q

Two bactericidal drugs that target different functions in combination:

What effects can they produce and what are 2 examples?

A

Additive or Synergistic Effects

  1. Penicillins can have additive or synergistic effects with aminoglycosides, which inhibit protein synthesis, against gram-negative bacilli such as P. aeruginosa, and against gram-positive enterococci and staphylococci
  2. Sulfamethoxazole and Trimethoprim inhibit sequential steps in bacterial folate synthesis and have synergistic activity against organisms that may be resistant to either drug alone.
36
Q

How can combination therapy reduce emergence of resistance organisms?

A

Need: Resistant Genes to both drugs to develop - Reduces changes.

Probility of Resistance to Drug 1 x Probability of Resistance Drug 2

.g., about 1 in 106 Mycobacterium tuberculosis organisms will
mutate to a resistant form during treatment with any single
drug. The rate of mutation to form resistant to two drugs is the product of the individual drug resistance rates, or about 1 in 1012 organisms. Because fewer than 1012 organisms are usually present in a patient with tuberculosis, it is unlikely that a resistant mutant will emerge during combination therapy. In the case of tuberculosis, combination therapy can delay emergence of resistance even though the drugs may not exhibit a synergistic effect against the microbe. 47

37
Q

What is Prophylactic Therapy?

A
38
Q

What do fungi exist as?

A
  • Yeasts (single cell, round)
  • Molds (multicellular filamentous)
  • Dimorphic Fungi (Combination)
39
Q

What are some characteristics with fungal infections?

A
40
Q

What are the contributing factors to why there has been of serious fungal infections since the 1970s?

A

Widespread use of broad-spectrum antibiotics, which eradicate the non-pathogenic bacterial populations that normally compete with fungi for nutritional resources.

Diseases causing compromised immune system, such as AIDS and the widespread use of immunosuppressants, and cancer chemotherapy agents.

Older people, people with diabetes, pregnant women and burn wound victims are particularly at risk of fungal infections such as candidiasis

41
Q

What are the different mechanisms of antifungals?

A

Damaging Cell Wall/Membrane
* Cell Wall synthesis Inhibitors
* Ergosterol Inhibitors

42
Q

What are 2 different antifungal drugs and what are the mechanisms of each?

A

Amphotericin B - Greater avidity for Ergosterol - Binding creates transmembrane ion channel, causing gross disturbances in ion balance with the loss of intracellular [K] altering cellular permeability and disrupting transport systems.

Clotrimazole - Broad Spectrum - Inhbit enzymes that produce ergosterol (CYP450)

43
Q

What is the main concern for Azole Antifungals?

A

Drug - Drug Interactions

A CYP450 inhibitor will reduce clearance of other drugs that are substrates for tha isozyme.

Result in: Decreased metabolism of Drug A Increased levels of Drug A in the body
44
Q

What are the structures of basic viruses?

A
  • A typical virus has a very simple structure:
  • Coat/envelope
  • Capsid
  • Genetic material (DNA/RNA)
  • Viruses typically rely on host cell structures to
    replicate.
  • The lack of available targets had presented a
    challenge to drug development.
    13
45
Q

What are the mechanisms in which antivirals work?

A
  • Target Viral Life Cycle
  • Target Replicative Machinery
46
Q

Explain the HIV lifecycle, where do drugs target, and some examples of drugs.

A

**Enfvirtide and Maraviroc: Viral Entry Inhibitors **

  • Is a 36-aa peptide that binds to gp41 and prevents
    its conformational changes that occur when HIV
    fuses with host cell membrane.
  • Can be combined with other antiviral agents.
  • Is costly and is only given subcutaneously (twice
    daily).
HIV Life Cycle Attaches CD4+ cells (via CD4 receptor + co-receptor). The Co-receptor: CCR5 or CXCR4. * Contains a reverse transcriptase to make cDNA. * Viral cDNA copy is integrated into host genome and form provirus. * Inactivates CD4+ cells, leading to deficient cell-mediated immunity. * Releases (bud off) without killing host cell. * After budding, the viral protease cleaves the viral protein precursors (maturation). 17
47
Q

What are common characteristics of different types of antiretrovirals and what are some examples?

A
  • Viral Entry Inhibitors: Enfuvirtide and Maraviroc.
  • Reverse Transcriptase Inhibitors (RTI) are subdivided into:
    ▪ Nucleoside (nRTI) - Competive inhibitors - compete for binding in growing chain.
    ▪ Non-nucleoside (nnRTI) - allosteric inhibition of enzyme
  • The Protease Inhibitors (PI) are the most toxic, but side effects have become more manageable.
  • The Integrase Strand Transfer Inhibitors (INSTI) are the newest antiretrovirals.
    ▪ Example: Raltegravir
48
Q

What is HAART?

A

Highly Active antiretroviral therapy.

Combination Therapy to reduce resistance.

Common Combos

49
Q

What type of antiretroviral has the most safety issues and what are they?

A

Protease Inhibitors

  • Hyperglycemia
  • Hyperlipidemia
50
Q

Antiviral treatment can last different periods of time

What are the different periods and what are some examples?

A

Few Days

Few Months - Hepatitus C

Lifelong - HIV

51
Q

What are the 3 major approaches for treating cancer?

A
  • Surgery
  • Radiation
  • Chemotherapy (Drugs)
52
Q

What are the hallmarks of cancer cells that make them easier to distinguish between normal cells?

A
  • Invasion and Metastases
  • Uncontrolled Proliferation
  • Establishment of Vascular Supply
  • Enhanced Survival Instinct
53
Q

What are cytotoxic drugs; what aspect do they target and what is the mechanism?

A

**Target Rapidly Dividing Cells **

Work by targeting - DNA sythesis or Mitosis.

**Neoplastics are cytotoxic drugs specifically for Cancer. **

Tissues inpacted by side effects

GI - Diarrhea, Ulcerations

Bone Marrow - Immunosupresion,Thrombocytopenia

Hair - Alopecia

Mitotic Mechanism

Microtubules play an important role in cell functions, particularly mitosis. *Facilitate the segregation of chromosomes during mitosis. They are composed of tubulins (α and β), and polymerization of tubulins allows it to grow. The taxanes bind to β-tubulins, preventing the microtubule from growing or shortening. This prevents mitosis from occurring, thus preventing cell division.
54
Q

What are characteristics of drugs that stop cancer growth instead of killing them and what is their mechanism?

A

Better at stopping and shrinking tumours.

Not curative option - Extend Life

Better Tolerated - Can take chronically - Oral

Example: Osimertinib - Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors. EGFR play important roles in cancer developement.

Mechanism

Tyrosine kinase receptors dimerize and initiate a series of intracellular signaling events that promote cell division. Inhibit This pathway by targeting these receptors (Targeted Therapy)
55
Q

How do angiogenesis inhibitors work and what are some examples?

A

Bevacizumab (Avastin) - Vascular Endothelial growth factor Inhibitor.

* Inhibiting angiogenesis * Like all tissues, cancers need blood supply * And they do this by stimulating angiogenesis
56
Q

What are 2 ways that cancer cells have a survival instinct to avoid Apoptosis?

A
  • Inhibiting Apoptosis
  • Repairing DNA
57
Q

What drugs inhibit cancers ability to inhibit apoptosis and what is the mechanism?

A

BH3 Mimetics - Venetoclax

Cancer cells prevent apoptosis by increasing expression of anti- apoptotic proteins like: bcl-2 (B-cell lymphoma 2) * Bcl-2 works by binding pro- apoptotic proteins like bax, preventing them from acting. In order to overcome this, we need to block bcl-2 The BH3 proteins are a family of proteins that facilitate apoptosis. * BH3 mimetics bind bcl-2 and prevent it from inactivating pro-apoptotic proteins like bax * And this promotes apoptosis.
58
Q

What drugs target Cancers ability for DNA repair preventing apoptosis and what is the mechanism?

A

PARP Inhibitors - Olaparib

* Poly ADP-ribose polymerase (PARP) senses DNA damage, * And facilitates DNA repair. * Therefore, PARP inhibitors prevent DNA repair from occurring... * And this promotes instability and cell death.
59
Q

Why does the immune system have a poor job in fighting cancer cells?

A

Cancer cells have a way of turning of the immune response.

Programmed cell death protein 1 (PD-1) * The PD-1 receptor is found on activated T- cells. * PD-L1 or PD-L2 is expressed on tumour cells. * PD-L1 on tumours binds to the PD-1 receptor –Turns off T-cell response to the tumour.
60
Q

What is an example of an immunotherapeutic agent for cancer and what is its mechanism?

A

Pembrolizumab

Pembrolizumab targets the PD-1 receptor, * Prevents PD from binding to the receptor, * T-cells then remain activated, and attack tumour cells. 49

CPPS 304 (11 decks)

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