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Host & Defense > Pharmacology-Host & Defense > Flashcards

Pharmacology-Host & Defense Flashcards

1
Q

What are the 5 classes of antimicrobials?

A
  1. Cell wall synthesis inhibitors
  2. Protein synthesis inhibitors
  3. Nucleic Acid inhibitors
  4. Metabolism inhibitors
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2
Q

What are the main cell wall synthesis inhibitors for antimicrobials?

A

Beta-lactam antibiotics (penicillin, carbapenem, cephalosporins, monobactams) and Vancomycin/Daptomycin/Polymixin B
-They work through the beta-lactam ring and interfering with transpeptidation reaction that seal the peptide cross-links between glycyn chains, they target PBP’s. But penicillases and beta-lactamases render them useless. Use a beta-lactam or 3rd generation ceph for CAP. Use Oral Penicillin V for pharyngitis, there has never been a case of resistance.

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3
Q

Which generation of cephalosporin enters the CNS?

A

3rd generation (ceftriaxone, cefotaxime). You use 3rd generation for gonococcus, pseudomonas, anaerobes, meningitis, gonorrhea, etc. You can use these for CAP.

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4
Q

Cephalosporins

A

Main toxicities are hypersensitivity reactions, toxicity of aminoglycosides, toxic with alcohol.

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5
Q

Beta-lactamase inhibitors

A

Like taxobactim, clavulonic acid, they help beta-lactams work better, they are suicide inhibitors, they are hydrolyzed by beta-lactamases for the antibiotics, so you add them with penicillin.

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6
Q

Vancomycin

A

Super toxic, effective against MRSA and C. diff. They depolarize bacterial cell-wall membrane, disrupt osmotic gradient, binding to D-ala. You get Red-Man Syndrome (severe flushing and rashes) as well as rhabdomyolysis. Along these lines, Daptomycin depolarizes the bacterial cell membrane, and Polymixins disrupts the osmotic gradient of the cell wall.

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7
Q

What are the main protein synthesis inhibitors for bacteria?

A

Buy AT 30, CCEL at 50. Numbers referring to ribosomal unit. A = aminoglycosides, T = tetracyclines, C = clindamyacin, C = Clarithromycin, E = Erithromycin, L = Linezolid. Aminoglycosides has frequent renal and oto-toxicity.

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8
Q

Clindamycin

A

Associated with C. diff overgrowth when used sometimes. It is a macrolide along with erythromycin. Use macrolides for atypical pneumonia.

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9
Q

What are the main nucleic acid synthesis inhibitors for bacteria?

A

Fluoroquinolones, which include ciprofloxacin and levofloxadin. As well as metronidazole and nitrofurantoin. Fluoros are mostly for gram negatives. Metro is good for anaerobes.

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10
Q

Fluoroquinolones

A

They inhibit DNA gyrase, toxicity includes tendonitis and tendon ruptures. Fluo got tendonitis trying to outrun a Flox. Use fluos for atypical pneumonia.

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11
Q

Metronidazole

A

Associated with C. diff overgrowth, it has free radicals that damage DNA, that is how it works.

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12
Q

Nitrofurantoin

A

Macrobid, damage DNA, helps kill E. coli in UTIs.

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13
Q

What are the main inhibitors of metabolism for bacteria?

A

Sulfonamides, TMP/SMX. Toxicity of these includes hemolysis if patient is G6PD deficient.

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14
Q

Rifampin

A

Drug used to treat leprosy and meningococcal infections. Inhibits DNA-dependent RNA polymerase, you can get red-orange body fluids.

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15
Q

Two main anti-pseudomonal antibiotics?

A

Pipercillin and Tazobactam

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16
Q

Beta-lactamases inactivate beta-lactam antibiotics. What inactivates aminoglycosides and macrolides?

A

Adenylases and Esterases.

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17
Q

What are the 4 different classes of antifungals?

A
  1. Membrane Function
  2. Ergosterol Synthesis
  3. Nucleic Acid Synthesis
  4. Cell Wall Synthesis
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18
Q

What are the two main drugs that target membrane function of fungi?

A

Amphotericin B and Nystatin. They are both polyenes, they bind to Ergosterol and form a pore that dirsupts membrane, allowing potassium to be lost and causing cell death. Toxicities include shake and bake syndrome, and 90% of people have renal effects of amphotericin B.

19
Q

What are the main ergosterol synthesis inhibitors for fungi?

A

Azoles, like fluconazole, ketoconazole, clotrimazole, and allylamines, they target the 14alpha-demethylase. Treat athles foot, candida. Fluconazole has good CNS penetration for fungal meninigitis. Terbinafine is the main allylamine. It inhibits squalene epoxidase in ergosterol synthesis. It is used for dermatophytes, but can be pretty hepatotoxic. Clotrimazole and nystatin can be used topically for vaginal candidiasis. Fluconazole is used as single oral dose usually effective for vaginal candidiasis.

20
Q

What are the main nucleic acid synthesis inhibitors for fungi?

A

Flucytosine, Griseofulvin. Flucytosine can have bone marrow suppression, and griseofulvin can be carcinogenic. The activity of griseofulvin is limited to dermatophytes.

21
Q

What is the main cell wall synthesis inhibitor for fungi?

A

Capsofungin, by inhibiting beta-glucan synthase.

22
Q

What are the main DNA viruses?

A

Adenovirus, Poxvirus, Herpes Virus, HPV.

23
Q

What helps block viral attachment and entry into a cell?

A

Entuvirtide, used for HIV.

24
Q

What helps block penetration of the mammalian cell once the virus is inside in the cytoplasm?

A

Interferon-alpha, which is used for HBV and HCV.

25
Q

What helps block uncoating of virus inside the cell?

A

Amantidine, binds to a protein M2, for influenza A, but not B.

26
Q

What helps block nucleic acid synthesis of virus in cell?

A

Acyclovir, used for HSV, and Foscarnet, used for CMV. With acyclovir you can get crystalline nephropathy. For genital herpes, three drugs are good with HSV. Acyclovir, foscarnet and trifluridine are active against strains of HSV. Foscarnet is not used in genital infections (HSV2) because it has poor oral bioavailability and trifluridine is used topically. So Acyclovir is best for oral dose.

27
Q

What helps block late protein synthesis and processing of a virus?

A

Protease inhibitors, used for HIV.

28
Q

What helps block the release of a virus from a cell?

A

Neuraminidase inhibitors like Osetlamivir (tamiflu), used for influenza A and B. The viral enzymes cleave sialic acid residues allowing for the viral release from the cell, so these antivirals stop these enzymes from doing so.

29
Q

What are the three eicosanoids?

A
  1. prostanoids
  2. Leukotrienes
  3. Lipoxins (anti-inflammatory)
30
Q

What are the three prostanoids?

A
  1. prostacyclins
  2. prostaglandins
  3. thromboxanes
31
Q

Name and describe the two main enzymes that help break down arachidonic acid:

A

Cox-1 and Cox-2. Cox-1 maintains balance of COX metabolites and is responsible for normal GI function. The expression of Cox-2 can be induced by pro-inflammatory stimuli like LPS, cytokines, growth factors. You can get peptic ulcers because of lack of mucous when you use NSAIDS, because PGE2 and I2, which come from Cox-1, help secrete mucous.

32
Q

Which enzymes do NSAIDS and Ibuprofen target?

A

They are non-selective for both Cox-1 and Cox-2. Can cause GI pain and nephrotoxicity. Linked with Stevens-Johnson syndrome.

33
Q

Which enzymes does Celebrex target?

A

It is selective for Cox-2, and this is good because there is less of a risk of a GI problem, but you can have heart issues with celebrex.

34
Q

How does aspirin work?

A

It works by irreversibly inactivating Cox-1 and Cox-2, and inhibits platelet aggregation. Is associated with postviral encephalitis (Reye’s syndrome) in kids. Aspirin can also cause Aspirin Exacerbated Respiratory Disease. Aspirin inhibits the formation of prostaglandins. PGEs (anti-inflammatory) inhibits/regulates the production of leukotrienes, so we end up getting too much leukotriene and causes excessive inflammatory responses.

35
Q

How does acetaminophen work?

A

It inhibits Cox-2 in the CNS, and is well tolerated.

36
Q

What is PGE1 used for when it is given?

A

It helps maintain the ductus arteriosus open in infants to help with PDA, can also help with ED, erectile dysfunction. Is also given to help induce contractions as misoprostol and is used to induce abortions.

37
Q

What is PGE2 used for when it is given?

A

You can treat glaucoma with it to increase outflow of aqueous humor, and dysmenorrhea is caused by increased endometrial synthesis of PGE2 so you can give NSAIDS to help with menstruation.

38
Q

How to relieve bronchoconstriction with drugs affecting eicosanoids?

A

You can use Zileuton, which inhibits lipoxygenase, so it inhibits leukotrienes (which are pro-inflammatory and too much can cause like asthma). Leukotriens are potent constrictors of airway smooth muscles. Also, montelukast inhibits CYSLT1 receptors to help with asthma.

39
Q

What are the four classes of immunosuppressants?

A
  1. Glucocorticoids
  2. Calcineurin inhibitors
  3. Antimetabolites/Anti-proliferative agents
  4. Biologicals (antibodies)
40
Q

What is the main drug with glucocorticoids with immunosuppressants?

A

Prednisone. It blocks cytokine activation by binding to corticosteroid response elements. Associated with cushings syndrome, hyperlipidemia, hyperglycemia, hypertension.

41
Q

What are the two main calcineurin inhibitors with immunosuppressants?

A
  1. Cyclosporine and 2. Tacrolimus. Cyclosporine works by blocking calcineurin, which usually dephosphorylates NFAT to make it active, which is essential to make IL-2, which is essential for T cells. Tacrolimus binds with FK-binding protein, and this complex inhibits calcineurin as well. Cyclosporin is lipophilic, and depends on bile for absorption. Cyclosporin is also associated with gingival hyperplasia.
42
Q

What are the three main drugs associated with antimetabolites/anti-proliferative agents in immunosuprresion?

A
  1. Azathioprine
  2. Mycophenolic acid derivatives (MPA)
  3. Sirolimus (rapamycin)
    - Immunosuppressants are usually never given as a single drug, they are usually combined with several in order to minimize side effects and they have different mechanisms that work together.
    - Sirolimus binds to mTOR, which inhibits T cell proliferation in response to IL-2.
    - Azathioprine and MPA are associated with myelosuppression, while sirolimus is associated with anemia, hyperlipidemia, and leukopenia.
43
Q

What are the main drugs that are antibodies and biologicals given for immunosuppression?

A
  1. Daclizumab
  2. Basiliximab
  3. Belatacept (I think this is like CTLA4-Ig
    - The first two above are antibodies that bind to and inhibit CD25 (IL-2alpha) on T cells
    - I think Belatacept is like CTLA4-Ig because it binds and blocks B7 on APC’s so they can’t interact with CD28.

Host & Defense (9 decks)

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