PHAR 100 > MODULE 4 > Flashcards

MODULE 4 Flashcards

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1
Q

selective toxicity

A

the use of drugs to harm the invading organism without harming the host

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2
Q

how is selective toxicity achieved

A

exploiting differences between the invading organism and human cells

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3
Q

antibiotic

A

a chemical substance that suppresses the growth of bacteria or eventually destroy them

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4
Q

bacteriostatic

A

inhibits the growth and reproduction of bacteria

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5
Q

bactericidal

A

directly kills the bacteria

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6
Q

bacteria structure

A

contains a cell wall containing a peptidoglycan layer that maintains cells shape and integrity

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7
Q

antibiotic classifications by spectrum

A
  • narrow spectrum: effective against particular species of microorganisms (penicillin G against Gram-positive)
  • broad spectrum: effective against wider range of microorganisms including both Gram neg and pos (e.g. tetracyclines)
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8
Q

cell wall synthesis inhibitors

A

Penicillins & Cephalosporins

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9
Q

Gram-Positive

A

bacteria that have a thick peptidoglycan layer and no outer membrane

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10
Q

Gram-negative

A

bacteria that have a thin peptidoglycan layer and have an outer membrane

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11
Q

cell wall synthesis inhibitors mechanism of action

A

function to stop the proper formation of the bacteria cell wall and/or membrane, influencing the structural integrity of the cell

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12
Q

DNA synthesis inhibitors mechanism of action

A

Inhibit DNA replication in bacteria, preventing bacterial growth

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13
Q

protein synthesis inhibitors mechanism of action

A

inhibit protein translation within bacteria and thereby protein synthesis

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14
Q

metabolic inhibitors mechanism of action

A

block the formation of key bacterial metabolic substrates needed for bacteria to survive and reproduce

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15
Q

cell wall synthesis inhibitors example

A

penicillins

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16
Q

Penecillin G

A

narrow spectrum antibiotic that destroys Gram positive bacteria.

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17
Q

what is Penicillin G useful for treating

A

pneumonia, middle ear infections, skin infections, and meningitis, and syphillis

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18
Q

penecillinase

A

enzyme that breaks down penicillin

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19
Q

methicillin

A

antibiotic resistant to attack by penicillinase

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20
Q

ampicillin and amoxicillin

A

broader spectrum. usefull against range of infections caused by gram-negative bacteria (e.g. uti)

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21
Q

amoxicillin and clavulanic acid

A

combination of a semisyntehtic penicillin plus an inhibitor of penicillinase that was introduced into therapy to combat penicillinase-producing strains of bacteria

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22
Q

penicillin mechanism of action

A

interferes with new bacterial cell wall formation and the resulting cells are formed without cell walls

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23
Q

what are cells called without cell walls

A

protoplasts

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24
Q

why is penicillin selectively toxic to bacteria

A

because human cells dont have cell walls

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25
penicillin adverse effects
GI distress due to disturbance of healthy gut flora, allergy
26
DNA synthesis inhibitors example
fluoroquinolones (ciprofloxacin)
27
Protein Synthesis Inhibitors example
Tetracyclines and Macrolides
28
Tetracyclines Mechanism of action
bind to the 30S subunit of the mRNA ribosome complex and prevent the addition of amino acids to the protein chain, inhibiting protein synthesis
29
Tetracyclines adverse effects
GI effects (nausea, vomiting, diarrhea), discolouration of teeth and diminished bone growth
30
why are tetracyclines used cautiously in pregnancy or children under 12
they have a strong affinity for calcium
31
why is it important to discard outdated tetracyclines
they can deteriorate into toxic degradation products
32
Macrolides use
- good for if someone is allergic to penicillin - active against Gram-pos
33
Macrolides Mechanism of Action
bind to the 50S ribsosomal subunit of trNA and block peptide bond formation
34
antifolates
metabolic inhibitors. inhibitors of folate metabolism in bacteria
35
tetrahydrofolic acid
essential for bacteria to synthesize DNA and protein
36
what will happen if tetrahydrofolic acid is not formed
bacteria growth will slow
37
sulfonamides and trimethorpim
both classified as antifolate drugs
38
Sulfamethoxazole-trimethorpim (co-trimoxazole)
treatment of uti, rtis, and gtis. combination of antifolates
39
when should antibiotics be used in combination
- severe infections when microorganism responsible isnt known or infection is so dangerous theres no time to find out - treatment of mixed bacterial infection - tuberculosis
40
why should antibiotics be mixed when treating tuberculosis
emergence of resistant mycobacterium is an important hazard
41
antimicrobials
agent that kills or inhibits growth of microbes. includes antibiotics, antifungals, antivirals, and antiparasitics
42
why does macteria become resistant to antibiotics
during replication, bacteria can mutate and evolve to have different properties
42
43
two major factors associated with development of antibiotic resistance
1. evolution of bacteria 2. clinical and environmental factors
44
causes of antibiotic resistance
1. over prescription 2. inappropriate use 3. use in agriculture
45
should you take antibioitcs for the flu? why?
no, because they are caused by viruses. taking antibiotics for the flu only contributes to the emergence of resistant bacteria
46
four mechanism for how bacteria become resistant to bacteria
1. uptake 2. target 3. inactivation 3. efflux pumps
47
uptake
small molecules gain access to the inside of the microorganism by moving through pores in the membranes. mutation or lack of these pores makes the organism resistant
48
target
a mutation in the target for the antibiotic can reduce the binding of the drugs to its target and be ineffective
49
inactivation
microorganisms develop an enzyme that inactivates the antibiotic. for example, the formation of penicillinase (inactivates penicillin)
50
efflux pumps
some microorganisms will over express transporters that pump the drug out of the microorganism before the cell cal be injured
51
two antifungal drugs
echinocandins and imidazoles (or azoles)
52
echinocandins mechanism of action
inhibiting the synthesis of a component of the cell wall, resulting in disruption of the cell wall and fungal death
53
two examples of echinocandins
micafungin and caspofungin
54
echinocandins route of administration
only available for intravenous administration
55
imidazoles mechanism of action
inhibit a fungal cytochrome p450, thereby inhibiting ergosterol synthesis
56
what is ergosterol critical for
fungal cell wall function and survival
57
virus
a small, infectious agent that is only able to multiply within living cells of other organism, including animals, plants, and bacteria
58
oseltamivir (tamiflu)
antiviral drug. it's a neuraminidase inhibitor used to treat influenza.
59
what is neuraminidase
an enzyme that allows the spread of the virus from cell to cell
60
acyclovir
taken up into infected cells, and the virus activates acyclovur to the active form. active acyclovir then inhibits viral DNA replication
61
when is acyclovir used
treatment of serious infections caused by herpes simplex virus. long term use of it will decrease the frequency of recurrence of genital herpes. also good for chickenpox and shingles
62
mechanism of action of hormonal contraceptive (inhibit hormone release)
inhibit release of gonadotrpin-releasing hormone (GnRH) from the hypothalamus. as result, the pituitary is not stimulated to release follicle-stimulating hormone and luteinzing hormone, resulting in no follicular maturation and the inhibition of ovulation
63
mechanism of action of hormonal contraceptive (inhibit sperm release)
contraceptives include progestins, which alter the secretions of the endocervical gland
64
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