PHAR 100 - Module 4 Flashcards

1
Q

antifungal → amophotericin B

A
  • drug of choice for severe fungal infection
  • binds to ergosterol, a steroid in the outer membrane of susceptible fungi that isn’t present in mammalian cells
  • pores form, causing leakage across fungal membrane
  • poorly absorbed from GI tract → administered via IV
  • kidney toxicity potential
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2
Q

antifungal → imidazoles (Azoles)

A
  • effective when taken orally for systemic fungal infections
  • inhibit a fungal cytochrome P450, inhibiting ergosterol synthesis
  • higher affinity for fungal P450 than human P450
  • can treat yeast infections
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3
Q

the viral lifecycle

A
  • take over operations of a cell in order to manufacture new viruses
  • specific in the types of cells they infect (receptor dependent)
  • instructions in virus DNA are transcribed to RNA
  • protein-building machinery of host cell translates these instructions into the components of a new virus
  • steps: 1) attachment, 2) entry, 3) replication, 4) biosynthesis, 5) assembly, 6) release
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4
Q

drugs for influenza → amantidine

A
  • inhibits the uncoating of viral DNA within infected cells, thereby preventing viral replication
  • used for prevention of influenza due to the influenza A virus
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5
Q

drugs for influenza → oseltamivir (Tamiflu)

A
  • a neuroamininidase inhibitor, which is an enzyme that allows the spread of virus from cell to cell
  • prevent neighbouring cells from getting sick
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6
Q

drugs for HSV/VZV

A
  • acyclovir inhibits DNA replication in infected cells
  • drug of choice for infections caused by herpes (HSV)
  • also useful in combatting infections due to varicella-zoster virus (VZV) - chicken pox and shingles
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7
Q

antibiotics

A
  • suppresses the growth of bacteria
  • purpose is to stop a bacterial infection
  • inhibits growth and reproduction of the bacteria (bacteriostatic effects) or directly kills the bacteria (bactericidal effects)
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8
Q

gram-positive bacteria

A

thick peptidoglycan layer and no outer membrane

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9
Q

gram-negative bacteria

A

thin peptidoglycan layer and an outer membrane

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10
Q

classification of antibiotics

A
  • classified based on the spectrum of microorganisms affected
    → narrow spectrum - only useful against particular species of microorganisms (penicillin G and gram-positive bacteria)
    → broad spectrum - effective against a wide range of microorganisms (tetracyclines)
  • and classified based on the biochemical pathway targeted in the microorganism
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11
Q

targets of antibiotics

A
  • cell wall and cell membrane synthesis
  • protein synthesis
  • nucleic acid metabolism
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12
Q

penicillins mechanism of action

A
  • target cell wall and cell membrane synthesis
  • interferes with new bacterial cell wall formation, and the resulting cells are formed without cell walls (protoplasts)
  • human cells don’t have cell walls and are unaffected
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13
Q

penicillins adverse effects

A
  • allergic reaction

- rash, diarrhea, fever

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14
Q

types of penicillin

A
  • natural: penicillin G (narrow spectrum, destroys gram-positive bacteria, used in pneumonia, middle ear infections, skin infections)
  • semisynthetic (modified penicillin G):
    → penicillin V (more stable with stomach acid, better for oral administration)
    → methicillin (is resistant to attacks by penicillinase)
    → ampicillin and amoxacillan (broader spectrum, useful agonist against a range of infections caused by gram-negative bacteria)
    → augmentin (combination of semisynthetic penicillin and an inhibitor of penicillinase, effective against penicillinase-producing strains of bacteria)
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15
Q

cephalosporins

A
  • more resistant to penicillinase than is the penicillin group
  • selective inhibitors of bacterial cell wall synthesis
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16
Q

penicillins and cephalosporins mechanism of action

A
  • in bacterial cell wall synthesis, an enzyme called a transpeptidase cross-links the 2 peptide chains using D-alanine-D-alanine in the reaction to form a strong, stable cell wall
  • penicillins and cephalosporins resemble D-alanine-D-alanine in structure and compete with them for the enzyme, and thus inhibit the enzyme
  • without cross-linking, the cell isn’t functional
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17
Q

fluroquinolones

A
  • inhibitors of bacterial DNA synthesis
  • ex: ciprofloxacin
  • can be used for oral or IV therapy of infections caused by gram-positive and negative microorganisms
18
Q

tetracyclines

A
  • inhibit protein synthesis
  • bind to the 30S subunit of the mRNA-ribosome complex and prevent the addition of amino acids to the protein chain
  • can have GI effects
  • diminished bone growth
19
Q

macrolides

A
  • inhibit protein synthesis
  • bind to the 50S ribosomal subunit on tRNA and block peptide bond formation
  • anorexia, nausea, vomiting
20
Q

antifolate drugs

A
  • inhibit protein synthesis
  • inhibit folate metabolism, which is essential for bacteria to synthesize DNA and protein
  • sulphonamides (competitively inhibit an upstream step in the synthesis of tetrahydrofolic acid by inhibiting para-aminobenzoic acid (PABA))
  • trimethoprim (inhibits dihydrofolic acid reductase, thus inhibiting tetrahydrofolic acid formation)
21
Q

antibiotic resistance

A
  • bacteria keep evolving
  • antibiotics are overused clinically and in the environment
  • patients aren’t finishing their treatment
22
Q

how organisms become resistant to antibiotics

A
  • mutations
  • increased efflux pumps
  • destruction of the antibiotic
23
Q

antibiotic combinations

A
  • appropriate for: therapy of a severe infection with an unknown microorganism, treating tuberculosis
  • disadvantages: unnecessary additional cost, increased chance of encountering toxicity
24
Q

the monthly ovarian cycle

A
  • at beginning of cycle, estrogen and progesterone levels in blood are low and endometrium is sloughed (menstruation)
  • in response to low levels, hypothalamus secretes gonadotropin-releasing hormone, stimulating pituitary to release FSH and LH
  • in response to FSH, ovarian follicles each containing 1 egg begin to enlarge
  • 1 of these follicles develops rapidly while others regress; maturing follicles secrete estrogen → endometrium thickens
  • day 14 → estrogen and FSH levels peak
  • follicle swells and releases ovum
  • fertilization occurs in transport to fallopian tube
  • corpus luteum releases progesterone
25
Q

mechanism of action of hormonal contraceptives

A
  1. release of gonadotropin-releasing hormone (GnRH) is inhibited from the hypothalamus; pituitary isn’t stimulated to release FSH and LH, resulting in no follicular maturation and ovulation is inhibited
  2. progestins alter the secretions of the endocervical gland to a scant, thick fluid not optimal for sperm migration
  3. endometrium is not fully developed and is unsuitable for implantation of a fertilized ovum
26
Q

oral contraceptives → fixed combination

A
  • fixed combo of estrogen and progestin, intended to be taken from the 5th-25th day of the cycle
27
Q

oral contraceptives → multiphasic

A
  • contain a fixed amount of estrogen and variable amounts of progestin (progestin increases from week to week)
  • currently the oral contraceptives of choice
  • hormonal sequence more closely mimics the pattern of hormones released in a normal ovarian cycle
28
Q

oral contraceptives → continuous

A
  • continuous estrogen and progestin preparations are taken for 28 days each cycle
  • menstruation is eliminated
29
Q

oral contraceptives → mini-pill

A
  • daily dose of progestin is taken as long as drug is needed

- spotting is common

30
Q

adverse effects of combination oral contraceptives

A
  • nausea, edema, headache
  • spotting, weight gain, acne, increased UTI
  • blood clots
  • heart attack
  • stroke
  • hypertension
  • reduced risk of cancer
31
Q

depo-provera

A
  • progestin-injected intramuscularly every 3 months

- spotting

32
Q

IUD

A
  • releases progestin, effective for 5 years
33
Q

norplant

A
  • comprised of silicone tubes filled with a progestin, which are implanted under the skin
  • drug is released over a period of 5 yrs
34
Q

transdermal patch

A
  • contain estrogen and progestin in a patch that’s applied to the skin
  • drug is delivered at a constant rate for 7 days
35
Q

post-coital contraceptives → estrogen

A
  • large dose of estrogen that are taken within 24 hrs after coitus
  • interferes with follicular development, alters cervical mucus, alter sperm migration, inhibiting fertilization
  • Plan B
36
Q

post-coital contraceptives → antiprogestins (Mifepristone)

A
  • blocks effects of the progesterone receptor in the endometrium
  • endometrium then lacks the support of progesterone, bringing on a period
37
Q

male contraceptives

A
  • try to control spermatogenesis
38
Q

androgen-based male contraceptives

A
  • androgens typically inhibit the release of GnRH, and thus spermatogenesis
  • in studies, levels of sperm count were considered infertile
  • enhances secondary sex characteristics, like aggression
39
Q

estrogen male contraceptives

A
  • suppress GnRH release and in turn spermatogenesis

- testosterone production and sex drive decreases

40
Q

progestin combined with androgen male contraceptives

A
  • progestin is used to inhibit the release of GnRH, results in a loss of spermatogenesis, decreased testosterone production and male secondary sex characteristics
  • androgens were added to replace lost testosterone and maintain secondary sex characteristics
  • finding appropriate dose of androgen is hard
41
Q

gossypol male contraceptive

A
  • compound obtained from cotton seed
  • destroys elements of the seminiferous tubules, decreasing sperm production
  • recovery of sperm count is not guaranteed