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PHPY 305 > Lixin Liu > Flashcards

Lixin Liu Flashcards

1
Q

Virus Particle (Virion) Components

A
  • Envelope
  • Core proteins (capsid)
  • RNA or DNA core (nucleois)
  • Surface proteins
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2
Q

Where do RNA viruses form their mRNA?

A

Cytoplasm except for influenza viruses

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3
Q

RNA retroviruses contain which type of DNA?

A

cDNA which are pro viruses that can be transcribed into new viral genomic RNA and mRNA

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4
Q

DNA viruses enter where?

A

Enter the nucleus to form viral mRNA

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5
Q

Viruses assemble these is the host cell

A

Virions which are released during cell lysis or budding (enveloped viruses)

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6
Q

DNA viruses blocking site?

A

Inhibition of viral DNA polymerase

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7
Q

RNA viruses blocking sites?

A

Block the uncoating, RNA polymerase, or the release of the virus

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8
Q

Neuraminidase inhibitors

A

Remove sialis acid receptors from viral particles and from cell surface, preventing self-aggregation and gluing to infected cell surface

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9
Q

Oseltamivir

A
  • oral
  • active prodrug
  • hydrolyses in the liver to active components
  • used for influenza A and B
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10
Q

Oseltamivir side effects

A

GI discomfort and nausea

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11
Q

Zanamivir

A
  • inhaled or intranasally or intravenous
  • contraindicated in patients with severe respiratory diseases or asthma
  • Influenza A and B use
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12
Q

Peramivir

A
  • intravenous only

- influenza A and B use

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13
Q

Peramivir adverse effects

A

Serious skin reactions

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14
Q

Amantadine and rimantadine action

A
  • blocks viral membrane matrix protein M2
  • viral uncoating inhibitors
  • Amantadine is effective in treating some Parkinson’s disease
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15
Q

Administration of Amantadine and Rimantadine

A

Orally for Influenza A only

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16
Q

Ribavirin used to treat

A
  • severe RSV in children
  • treatment of influenza
  • chronic hepatitis C infections
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17
Q

Ribavirin action

A

Inhibits GTP formation, viral mRNA capping, and thereby inhibits viral protein synthesis

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18
Q

Ribavirin routes of administration

A
  • oral
  • IV
  • aerosol
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19
Q

Interferon mode of action (3)

A
  • induction of host cell enzymes that inhibit viral RNA translation
  • degradation of viral RNA
  • stimulation of immune system
  • for treatment against hepatic viral infections
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20
Q

Interferon route of administration

A

Intralesionally, subcutaneously, or intravenously

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21
Q

Interferon adverse effects

A

Flu-like symptoms, bone marrow suppression, neurotoxicity, autoimmune disorders

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22
Q

Lamivudine mode of action

A

Inhibits both HBV DNA polymerase and HIV reverse transcriptase
- for treatment of HBV and HIV

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23
Q

Lamivudine route of administration

A

Orally

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24
Q

Acyclovir treatment of

A
  • drug of choice for HSV types 1 and 2 as well as VZV
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25
Q

Acyclovir route of administration

A

IV, oral, and topical

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26
Q

Acyclovir mode of action

A
  • competitive inhibition of dGTP for viral DNA polymerase
  • binding to DNA template, causing termination of premature viral DNA
  • trapping the viralDNA polymerase on acyclovir-terminated DNA chain
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27
Q

Adverse effects of Acyclovir

A

Depends on the route of administration

  • Topical: local irritation
  • Oral: headache and GI upsets
  • IV: transient renal dysfunction at high dose
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28
Q

Nucleoside and Nucleotide Reverse Transcriptase Inhibitors (NRTI’s)

A
  • pro drugs
  • convert to the triphosphates in the cell
  • incorporated by viral reverse transcriptase into viral DNA to terminate its elongation
  • Have much lower affinity to host cell DNA polymerase but affect mitochondria DNA polymerase in certain tissues
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29
Q

Zidovudine

A

Converted by mammalian thymidine kinase to triphosphate introduced by viral reverse transcriptase into viral DNA
- Used in HAART, decreases viral load and increases CD4+ cells. Also used for prophylaxis

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30
Q

Zidovudine route of administration

A

Orally administered, glucuronylated by the liver

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31
Q

Zidovudine adverse effects

A

Toxic to bone marrow, headaches, toxicity can be potentiated by other drugs

32
Q

Nevirapine (NNRTI) adverse effects

A

Rash can be severe
Fatal hepatotoxicity can occur
Induces CYP3A4 of cytochrome P450 enzymes, and metabolism of a number of other drugs

33
Q

Efavirenz

A
  • only used in combination with other HIV-1 agents
  • Very potent against HIV-1
  • Preferred treatment with addition of 2 NRTI’s.
    Efavirenz + Tenofovir + Emitricitabine (once daily co-formulation single pill).
34
Q

Protease inhibitors adverse effects

A

GI intolerance, disturbances in glucose and lipid metabolism
- diabetes, hypertriacylglycerolemia, hypercholesterolemia, and fat redistribution

35
Q

Ritonavir

A
  • Inhibits CP450 isozymes and is one of the most known potent inhibitors of CYP3A4
  • inhibits the metabolism of all current HIV PIs and is frequently used in combinations with most other PIs
  • “Pharmacokinetic enhancer”
36
Q

Saquinavir

A
  • poor bioavailability
  • must be taken with high fats
  • GI upsets are common
37
Q

Viral Entry Inhibitors

A

Enfuvirtide and Maraviroc

38
Q

Enfurvitide

A
  • inhibits viral fusion
  • 36 aa peptide that binds gp41 and prevents its conformational changes that occur when HIV fuses with host cell membrane
  • can be combined
  • costly and only give subcutaneously twice daily
39
Q

Maraviroc

A

CCR5 antagonist

- restricted to use in adults with CCR5-tropic HIV-1

40
Q

CCR5

A

Major co-receptor involved in viral entry into the cell

41
Q

Integrate inhibitors

A

Raltegravir, Dolutegravir and Elvitegravir

42
Q

Raltegravir route of admin.

A

Oral

43
Q

Raltegravir mode of action

A

Inhibits HIV-1 integrate activity preventing viral DNA from integrating with cellular DNA. It is active against HIV strains resistant to other anti-retroviral drugs.

44
Q

Immunosuppressive Drugs

A

Are used to dampen the immune response in organ transplantation and autoimmune diseases, and to suppress inflammatory reactions

45
Q

Immunostimulatory Drugs

A

Applicable to the treatment of infection, immunodeficiency, cancer

46
Q

Cardinal signs of Acute Inflammation

A 
Redness (rubor)
Heat (calor)
Swelling (tumor)
Pain (dolor)
Loss of function
47
Q

Cellular events in inflammation

A
  1. Leukocyte extravasation
  2. Cell activation, exocytosis, and phagocytosis
  3. Release of leukocyte products and leukocyte-induced tissue injury
    - lysosomal enzymes
    - reactive oxygen intermediates
    - products of arachidonic acid metabolism
48
Q

Cytokines include:

A
  • Interleukins
  • Interferons
  • Tumor necrosis factors
  • Transforming growth factors
  • Colony-stimulating factors
  • Chemokines
49
Q

Glucocorticoids mechanism of action

A
  • regression of lymphoid tissues
  • enhance destruction of lymphocytes (especially T lymphocytes)
  • interfere with the cell cycle of activated lymphoid cells
  • inhibit leukocyte functions
  • inhibit antibody formation
  • inhibit inflammatory mediators
50
Q

Prednisone mechanism of action

A
  • represses COX-2 gene and enzyme expression
  • represses the expression of cytokines that activate COX-2
  • blocking the function of Phospholipase A2 therefore limiting the availability of arachidonic acids
51
Q

Glucocorticoids clinical uses

A
  • organ and tissue transplantation
  • autoimmune diseases (drug of choice)
  • inflammatory diseases (allergies, arthritis, bowel disease)
52
Q

Glucocorticoids Adverse Effects

A

Suppression of pituitary-adrenal axis
Increased susceptibility to serious infection
Peptic ulcer

53
Q

Cyclosporine action

A
  • binds to cyclophiln, inhibits calcineurin, which inhibits NFAT from going into the nucleus to produce IL-2
  • inhibits cytokines production
54
Q

Cyclosporine AE’s

A
  • Nephrotoxicity
  • Hepatotoxicity
  • Prédispose to infections
  • lymphoma may occur
  • hypertension, hyperkalemia, tremor, hirsutism, glucose intolerance, and gum hyperplasia
  • causes little bone marrow toxicity
55
Q

Tacrolimus action

A
  • more potent and allows lower dose of glucocorticoids to be used
  • binds to different immunophilin (FKBP-12)
56
Q

Sirolimus action

A
  • also binds FKBP-12 forming a complex with mTOR
  • Sirolimus binding to mTOR blocks the progression of activated T cells from the G1 to the S phase of cell cycle, consequently the proliferation of these cells
57
Q

Methotrexate mechanism of action

A
  • antagonist by inhibiting dihydrofolate reductase which converts folic acid into tetrahydrofolic acid
  • decreases biosynthesis of A, T, C, G and eventual death of the cell
  • Immunosuppressive antimetabolite
58
Q

Leflunomide mechanism of action

A
  • reversible inhibits dihydroorotate dehydrogenase and deprives the cells of the precursor for uridine monophosphate
  • reduces pain and inflammation associated with the disease, slows the progression of structural damage
  • immunosuppressant antimetabolite
59
Q

Mechlorethamine mechanism

A
  • causes lymphocytopenia
  • alkylate the N-7 nitrogen of a guanine residue in one or both strands of DNA
  • largely replaced by cyclophosphamide
  • Immunosuppressive alkylating agents
60
Q

Cyclophosphamide

A
  • the most commonly used alkylating agent
  • biotransformed into the active compound, phosphoramide mustard, which alkylate DNA.
  • Immunosuppressive alkylating agent
61
Q

Types of Antibodies (4)

A
  1. Polyclonal antibodies
  2. Monoclonal antibodies
  3. Humanize antibodies
  4. Chimeric antibodies
62
Q

Antithymocyte globulins

A
  • purified polyclonal Abs from rabbit
  • treat acute renal transplant rejection
  • depletion of T cell responses
  • humoral antibody mechanism remains active
63
Q

Muromonab-CD3

A
  • murine mAbs, for the depletion of human T cells
  • used in autoimmune disorders and renal, cardiac and hepatic transplant as well as depletion of T cells from the donor bone marrow
64
Q

Antithymocyte globulins and Muromunab-CD3 adverse effects

A
  • Cytokines release syndrome

- using humanize anti-CD3 mAb can minimize this effect

65
Q

Intravenous Immunoglobulins treatment

A
  • treats Ig deficiencies, AIDS, autoimmune disorders, and bone marrow transplants
  • prepared as IgG
66
Q

Hyperimmune Immunoglobulins

A
  • treatments against viruses or toxins
  • syncytial virus, cytomegalovirus, varicella zoster virus, human herpesvirus type 3, HBV, rabies, tetanus, and digoxin overdose
67
Q

Omalizumab mechanism

A
  • anti-IgE recombinant humanize mAb blocking the binding of IgE to Fce receptor
68
Q

Omalizumab treatment

A
  • allergic asthma patients whose symptoms are refractory to inhaled corticosteroids
69
Q

Basiliximab and daclizumab

A
  • humanized mAbs
  • use with CSA and glucocorticoids
  • both are anti-CD25 mAbs (bind to alpha chain of the IL-2 receptor on activated T cells).
  • Are used for prophylaxis of acute organ rejection in adult patients
70
Q

Infliximab

A

Chimeric antibody

TNFalpha antagonist

71
Q

Adalimumab

A

Humanized antibody

TNFalpha antagonist

72
Q

Etanercept

A
  • fusion protein comprising part of TNF p75 receptor and the Fc portion of human IgG.
  • Binds to TNFalpha and lymphotoxin
  • TNFalpha antagonist
73
Q

Anti-TNF AE’s

A
  • reaction at injection site
  • infections
  • malignancies
  • cardiac failure
74
Q

Anakinra

A
  • recombinant form of IL-1 receptor antagonist

- differs by a methionine residue

75
Q

Anakinra AE’s

A
  • similar to TNFalpha antagonists
  • asthma may be a co-morbid risk factor for serious infections
  • use of anakinra and etanercept increases risk of neutropenia and serious infections

PHPY 305 (14 decks)

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