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Big Pharma > Pharm Quiz 6 > Flashcards

Pharm Quiz 6 Flashcards

1
Q
  1. What are the mechanisms of action that antibacterial medications work?
A
  • Inhibition of bacterial cell wall synthesis and function
  • Inhibition of bacterial protein synthesis
  • Inhibition of bacterial DNA/RNA function
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2
Q
  1. What proteins do penicillins exert their effect by inhibiting the function of? This results in the impaired production of what is essential for normal membrane structure and function?
A
  • Penicillin-binding proteins
  • This inhibits the normal synthesis and organization of the bacterial cell wall; PBPs manufacture the peptidoglycans which are essential for normal membrane structure and functions. Therefore the construction of the bacterial cell wall is impaired, and the cell dies from the membrane’s inability to serve as a selective barrier and to contain the high internal osmotic pressure of the bacterial cell
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3
Q
  1. How do aminoglycosides work? What part of the bacterial cell do they impair?
A
  • Work by inhibiting or impairing the synthesis of bacterial proteins responsible for various cellular functions, including enzymatic reactions and membrane transport
  • Impairs bacterial cell membrane transport and metabolic function, resulting in retarded growth or death of the bacteria
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4
Q
  1. Sulfonamide drugs selectively inhibit the synthesis and function of the nucleic acids and certain amino acids by impairing the production of what in the bacterial cell?
A

Inhibiting the production of folic acid

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5
Q
  1. Why are beta-lactamase inhibitors combined with specific penicillins?
A

Beta-lactamase inhibitors are typically combined with a specific type of penicillin or other beta-lactam agent to treat infections caused by bacteria that produce beta-lactase enzymes. The beta-lactamase inhibitor prevents the enzymes from destroying the penicillin thus allowing the penicillin to remain intact and effective against the bacterial infection

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6
Q
  1. What antibiotic is tendon pain and inflammation a side effect of that can lead to tendon rupture?
A

Fluoroquinolones

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7
Q
  1. How do bacteria become resistant to antibacterial medications?
A

Certain bacterial strains have a natural or acquired defense mechanism against specific antibacterial drugs. This enables the strain to survive the effects of the drug and continue to grow and reproduce similar resistant strains, thus representing a genetic selection process in which only the resistant strains survive the drug

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8
Q
  1. Why should UV light therapy in rehabilitation interventions be used cautiously with certain antibiotics?
A

Hypersensitivity reactions can occur

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9
Q
  1. Should broad spectrum or narrow spectrum antibiotics be used to limit bacteria resistance to drug therapy?
A

Narrow spectrum

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10
Q
  1. Why are viral infections more difficult to treat than bacterial infections?
A

It is difficult to selectively destroy the virus without also destroying human cells

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11
Q
  1. How do reverse transcriptase inhibitors work?
A

Impair HIV replication by inhibiting the reverse transcriptase enzyme that is needed to convert viral RNA to viral DNA

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12
Q
  1. HAART (Highly Active Antiretroviral Therapy) consists of what drugs?
A

Simultaneous use of at least 3 anti-HIV agents

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13
Q
  1. How can reverse transcriptase inhibitors impact your work with a patient? (think SEs that would impact therapy)
A

RTIs may cause myopathy, as indicated by skeletal muscle tenderness, weakness, and atrophy. Likewise, peripheral neuropathies, liver dysfunction, and lactic acidosis may also occur. Neuromuscular problems are seen frequently.

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14
Q
  1. What are interferons?
A

a group of proteins that are synthesized as part of the immune response to viral infection, and these substances enable healthy cells to resist infection from a wide array of viruses. Interferons produce other beneficial effects, including the control of cell differentiation, the limiting of excessive cell proliferation, and the modification of certain immune responses.

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15
Q
  1. How are antiviral vaccines created?
A

3 Main Types of Antiviral Vaccines
- Live attenuated: MMR, Varicella, Herpes Zoster
- Inactive: Polio, Rabies, Influenza, Pneumococcal, Dpt
- MRNA: COVID-19 vaccine (Pfizer)

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16
Q
  1. How are cutaneous and mucocutaneous infections such as ringworm typically treated?
A

Topical antifungal agents (azoles)

17
Q
  1. What are reasons that systemic fungal infections could be more severe in one patient versus another?
A

Compromised immune status

18
Q
  1. Why are some malarial drug treatments ineffective in some parts of the world?
A

Resistance to this drug, however, has emerged in many regions where malaria is prevalent. That is, the parasite that causes this disease (the Plasmodium amoeba) has developed mechanisms that render this drug ineffective

19
Q
  1. What class of drugs treat tapeworms, roundworms, and flukes?
A

Anthelmintics

20
Q
  1. Is the risk of liver toxicity with antifungal drugs more significant with oral or topical administration?
A

Oral administration

21
Q
  1. Many antifungal drugs selectively affect fungal cells rather than human cells by impairing what part of the fungal cell membrane?
A

Antifungal drugs typically impair fungal cells by disrupting membrane function, impairing RNA and protein synthesis, or inhibiting mitosis.

Many of these drugs impair the production of membrane sterols, triglycerides, and phospholipids.25 Loss of these components results in the membrane’s inability to maintain intracellular homeostasis, leading to the death of the fungus.

22
Q
  1. Describe how anticancer medications work that are classified as cell cycle nonspecific.
A

Cell-cycle–nonspecific exert antineoplastic effects on the cell regardless of the cell cycle’s phase. Examples of cell-cycle–nonspecific agents include most alkylating agents and antineoplastic antibiotics.

23
Q
  1. What medication categories are used to treat cancer?
A

Specific anticancer agents:
- Alkylating Agents
- Antimetabolites
- Anticancer Antibiotics
- Antimicrotubule Agents
- Topoisomerase Inhibitors
- Anticancer Hormones

Targeted and Biological Therapies:
- Monoclonal Antibodies
- Cytokines
- Tyrosine Kinase Inhibitors

Platinum Coordination Complexes
Aspirin and Other NSAIDs

24
Q
  1. Why are monoclonal antibodies especially effective in treating certain cancers?
A

Monoclonal antibodies are manufactured using cell cloning techniques that produce an antibody that is specific for an antigen on the surface of a particular type of cancer cell.

25
Q
  1. What is the relatively new strategy for treating certain tumors that prevents the formation of new blood vessels called?
A
  • Angiogenesis inhibitors
  • These agents inhibit the formation of new blood vessels in growing tumors.
26
Q
  1. What is inhibited by administering NSAIDS that may help to prevent colorectal cancer and other malignancies?
A

Platelet formation

27
Q
  1. Why are the side effects of most anticancer medications severe and potentially toxic? (hint: think about what cells in the body these medications affect)
A

Although cancer cells have become more primitive and have lost much of their normal appearance, they are still human cells that have simply gone wild; they cannot be easily destroyed without also causing some harm to healthy human tissue.

28
Q
  1. How do the newer cancer chemotherapy agents called biologic therapies work?
A
  • Biological therapies or biological response modifiers because they encourage the body’s immune system to fight cancerous cells. Targeted and biological therapies offer the potential advantage of impairing function in cancer cells with minimal effects on healthy human cells.
  • These therapies include monoclonal antibodies, cytokines (interferons, interleuklin-2), and tyrosine kinase inhibitors.
29
Q
  1. What are the reasons that medications are used to suppress the immune system?
A

2 main reasons:
- prevent rejection of organ/tissue transplants
- suppression of an autoimmune response

30
Q
  1. What medication examples are used to suppress the immune system?
A
  • Azathioprine (Imuran)
  • Cyclophosphamide (Cytoxan)
  • Cyclosporine (Neoral)
  • Glucocorticoids: hydrocortisone
  • Methotrexate
  • Mycophenolate Mofetil (CellCept)
  • Sulfasalazine (Azulfidine)
  • Sirolimus
  • Tacrolimus (Prograf)
31
Q
  1. Why is sirolimus a good drug choice following a kidney transplant?
A
  • Sirolimus and its analogs do not interfere directly with cytokine production. these drugs inhibit the function of mTOR.
  • By inhibiting mTOR, these drugs cause cell division to stop at a specific stage (G1), thereby limiting the ability of these cells to mount an attack on transplanted tissues
32
Q
  1. Cyclosporine is commonly used to prevent organ rejection. Why is it modified into microemulsion capsules for administration?
A
  • The drug is modified into microemulsion capsules that disperse more easily within the GI tract, thereby enabling the drug to be absorbed in a more predictable fashion.
  • The microemulsion form of cyclosporine appears to be safer because it is not as toxic to the kidneys and other tissues as is the regular formulation.
33
Q
  1. Cyclosporine suppresses the immune function by inhibiting what protein in the lymphoid tissues? Does this decrease the production of what cytokine signaling molecule in the immune system?
A
  • Cyclosporine inhibits a specific protein (calcineurin) in lymphoid tissues.
  • suppresses T-cell activation, thus limiting the ability of T cells to produce other chemical mediators that promote immune cell activity
34
Q
  1. What are the long-term risks/side effects of using glucocorticoids to suppress immune function following organ transplant?
A
  • Adrenocortical suppression
  • Breakdown of supporting tissues (muscle, bone, ligaments, tendons, skin)
  • Peptic ulcer formation
  • Glaucoma
  • Mood changes and psychosis
35
Q
  1. What medical procedure long term are medications that block interleukin 2 receptors and prevent activation of T lymphocytes especially helpful?
A

Organ transplants

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