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
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
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
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
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
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
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)
8
Q
gram-positive bacteria
A
thick peptidoglycan layer and no outer membrane
9
Q
gram-negative bacteria
A
thin peptidoglycan layer and an outer membrane
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
11
Q
targets of antibiotics
A
- cell wall and cell membrane synthesis
- protein synthesis
- nucleic acid metabolism
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
13
Q
penicillins adverse effects
A
- allergic reaction
- rash, diarrhea, fever
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)
15
Q
cephalosporins
A
- more resistant to penicillinase than is the penicillin group
- selective inhibitors of bacterial cell wall synthesis
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
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
- 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
- progestins alter the secretions of the endocervical gland to a scant, thick fluid not optimal for sperm migration
- 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
