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pharm exam 2
Terms in this set (322)
which of the following affect(s) the development of antimicrobial resistance?
d-all of the above
moxifloxacin is a group ______ quinolone
"environmental resistance" of a bacterial isolate means that
a-the bacterium in question has been isolated from animals
b-the bacterium in question is resistant to agricultural chemicals
c-the bacterium in question is a non-pathogenic strain
d-the bacterium in question is a pathogenic strain
superinfection can occur in
a-the oral cavity
b- the genitourinary tract
c- the bowel
d-all of the above
which of the following is TRUE?
a-europe has the highest incidence of antibiotic residue in meat
b-organic farms don't harbor resistant bacteria
c-it is difficult for bacteria to acquire resistance by conjugation
d-conventionally farmed meat in the USA has the highest antibiotic residue in the world
antibiotic resistance has reached such alarming proportions that the WHO has issued advisories about this
many cephalosporins are ___________
a-broad spectrum antibiotics
b-related to fluoroquinolones
c-in the 5th generation
d-all of the above
first generation cephalosporins ____________
a-have some gram (-) coverage
b-are not useful for dental applications
c-have very good gram (-) coverage
d-are active against MRSA
in which case would you avoid using beta lactams for a dental patient?
a-the pt has had dyspepsia with penicillin treatment
b-the pt has experienced diarrhea with cephalosporin treatment
c-the pt has experienced rashes with cephalosporin treatment
d-the pt has had hives or an episode of anaphylactic reaction with penicillin treatment
a-requires months of treatment to eliminate the infection
b-infection can occur outside the lungs
c- is a special kind of infection to treat
d- can remain latent in the body for years
e-all of the above
latent TB infection
a-status is always known by the patient
b-can reactivate with immunosuppressive therapy
c-represents a risk factor for treating a dental patient
d- can always be prevented by vaccination with BCG
rifampin is ___________ agent to treat TB
a-a second line
b-unsafe in pregnant patients as an
d-a first line
a-inhibits M. tuberculosis cell wall synthesis
b-is effective alone to eliminate MDRTB
c- cannot be used for TB prophylaxis
d-is a second line agent for treating TB
are "antimicrobial agents" and "antibiotics" the same thing?
what's the difference between an antibiotic and an antimicrobial?
ANTIBIOTIC: produced by organisms
ANTIMICROBIAL: all chemical, natural or synthetic (human-made)
the first natural antibiotic ever created was ___________
the first synthetic antimicrobial that was synthesized was ____________
antibiotics can be bactericidal or bacteriostatic.... what's the difference?
what's tricky about both?
CIDAL: kills the microorganisms (so it needs to be actively growing)
STATIC: stops the growth of the microorganisms (doesn't get rid of them, so you'll need a competent immune system to rid the organisms)
with __________ antibiotics, the microorganisms must be actively growing in order to be effective
what does it mean that antimicrobial drugs have a selective toxicity?
they're able to kill the target cells without injuring the host cells
what are 4 main ways that selective toxicity is accomplished (aka how are just the bacteria targeted, and not the host cells)?
-disrupt the bacteria cell wall
-inhibit enzymes unique to bacteria
-disrupt bacteria protein synthesis
-inhibit bacteria nucleic acid synthesis
cephalosporins and penicillins have selective toxicity by targeting the bacteria cell wall... how does targeting the bacteria cell wall cause death?
with a weakened cell WALL, (vs. mammalian cell membranes ) the bacteria absorb water, burst, and die
sulfonamides are bacteriostatic and suppress bacterial cell growth by inhibiting an enzyme necessary for bacterial growth called _________________
is each usually bacteriostatic or bacteriocidal?
antibiotics who accomplish selective toxicity by:
-disrupting bacteria cell wall
-inhibit bacteria enzymes
-disrupt bacteria protein synthesis
-inhibit bacteria nucleic acid synthesis
true or false
Bacteria have a different type of ribosomes which can be selectively inhibited by antibiotics such as aminoglycosides or tetracyclines
what are 2 examples of antibiotics that interfere with enzymes required for nucleic acid synthesis?
rifampin and fluoroquinolones
what's the difference between narrow and broad spectrum antibiotics?
N: active against only a few microbes
B: active against a wide variety of microbes
between broad and narrow spectrum antibiotics:
which is best to use?
which may cause resistance?
which may prevent resistance?
which can lead to superinfections?
which can also kill beneficial/commensal bacteria?
-broad (note: commensal bacteria just means the normal flora of beneficial bacteria)
what is a superinfection (aka suprainfection)?
why does this happen?
-a new infection that emerges during treatment (so a new infection occurring during current antibiotic treatment)
-because the antibiotic attacks the good (protecting) bacteria too, so there is an imbalance for bad bacteria to invade
what are some examples of a superinfection?
- Clostridium difficile (a.k.a. C. diff )
-Oral Candidiasis (lay term = thrush)
true or false
about 15,000 people die every year in the US from Clostridium difficile (a bacteria that overtakes due to antibiotic use.... so a superinfection)
has resistance always existed in nature?
yes, since microorganisms have always made chemicals advantageous for their survival..... so resistance is natural and always evolving
how long does it take most bacteria to replicate/double?
why do we care?
-an hour or two
-this makes it so that they are able to rapidly evolve
true or false
drug resistant infections kill 35,000 people a year (1 every 15 minutes)
what is a major reason why new antibiotics aren't being developed to treat drug resistant disease?
why have major developers gotten out of the business of antibiotic development?
why do major drug companies want to make drugs for things like diabetes, rather than antibiotics?
money (with antibiotics, the pt pays for it one time, since it's single use then you're good) (with diabetes the pt is paying for new insulin every day, so much more of a money maker)
according to the CDC in 2019, which 2 bacteria are urgent threats? which 2 are serious threats? which 1 is a concerning threat?
U: Candida auris; Carbapenem resistant Enterobacteriaceae
S: Drug resistant Streptococcus pneumoniae; Drug resistant tuberculosis
C: Clindamycin-resistant Group B Streptococcus
what is a resistome?
group of all existing antibiotic resistance genes (known or unknown) in the world
what's the difference between acquired resistance and innate resistance?
A: the microbe has an antibiotic resistant gene which is not present in other related bacteria (this is a huge clinical problem!)
I: the antibiotic resistance gene is common to all related bacteria (present within the chromosome) (passed on when the bacteria divides)
what is the difference between environmental and clinical resistance?
E: resistance in a non-pathogenic strain of bacteria
C: resistance in a pathogenic strain of bacteria
which antibiotics given, will create selective pressure by killing sensitive organisms, and favoring survival of resistant organisms?
all antibiotics do this
(the bacteria that survive can now access the nutrients that were formerly being used by the sensitive bacteria)
bacteria can get acquired resistance through two ways... describe each
which is the most dangerous?
SPONTANEOUS MUTATION: random DNA changes, usually creating a resistance to just one drug
BACTERIAL CONJUGATION: transfer of resistance genes (extrachromal DNA) using a sex pili; occurs in gram negative bacteria and can lead to resistance to multiple drugs
*conjugation is more dangerous since it spreads quicker and is resistant to multiple drugs
which is more dangerous: spontaneous mutation or bacterial conjugation?
selective pressures help to create drug resistance, such as clinical, social, and at home
describe how each does this
C: inappropriate prescribing
S: non-prescription use when antibiotics are readily available (ex: Asia, S. America, other countries)
AH: people buy antibacterial hand soaps
why should you never buy antibacterial hand soap?
-kils 99% and 1% survive, this just further encourages antibiotic resistance of the 1%
-Just use normal soap and water and that will be enough
food production in the US accounts for ____% off all antibiotic usage (so animals use more antibiotics than people)
however most if that isn't to fight infection... so how is it used?
-used for growth promotion... antibiotics are used to overcome the unsanitary living conditions, but any energy that isn't used to fight infection goes to putting on weight faster (bigger animals=more money)
true or false
antibiotics are useful in animals, however they're not used for plants
they are also used for fruit/vegetables/trees/etc. plus the manure they're usually farmed in is laden with antibiotics
what is an MGE (mobile genetic element)?
a type of DNA that can move around in the genome, or be transferred to a recipient organism
Antibiotics that are not degraded by microbial action persist in soil, leach into water, and into runoff from fields and thus ultimately into ___________________________
human community water supplies.
what are 2 examples of quaternary ammonium compounds?
are these good or bad? why?
-Clorox Disinfecting Wipes (which don't actually have clorox in them) & Lysol
-bad, they allow 1% of organisms to survive, now this 1% can become antibiotic resistant
what should you use instead of disinfecting wipes or lysol or anything that kills only 99% of bacteria?
-alcohol based cleaners instead (ex. Purell) because this will kill 99% of organisms, then dehydrate (and thereby kill) whatever is left... so there's nothing remaining to multiply and become resistant
what is transduction?
what is transformation?
what is conjugation?
T: using a bacteriophage
T: capsule of genes that was incorrectly packaged upon plasmid excision
C: transfer of genes via a sex pili
1 in every 1 million bacteria is considered to be a "persister cell"
what does this mean?
-it survives antibiotic treatment (bactericidal and bacteriostatic) and remains dormant and hides out (ex in a macrophage)... then once these sleeper cells reactivate, ex: once antibiotic treatment stops, they might have created a much more favorable environment for another bout of infection, or even a completely new infection from another bacteria or virus
to avoid creating antibiotic resistance, you should use antibiotics for the recommended ______________
do not prescribe for ________ infections
use _________ spectrum first
use __________ generation first
evenly spaced out _________
-dosages (to maintain therapeutic levels)
there are three hygienic practice types... describe each
B: clean food/water; distancing from infected people
E: hand washing; sterile surgeries; chemically treating wounds/disease
SS: use of hand sanitizer; antibiotic mis-use; sterilizing random surfaces
what are the 3 types of hygienic practices?
how does each affect virulence levels?
Baseline: encourages lower virulence levels
Extended: keeps virulence levels constant
Super Sanitization: encourages higher virulence levels (dangerous)
what is potency?
what is the minimum inhibitory concentration?
P: drug concentration needed to get an effect
MIC: amount of drug required to produce a given % of its Emax
what does it mean that a drug can be very potent, but poorly efficacious?
-a drug can be very effective at low doses, but the response may not change even when the dose is increased.
-thus, drug potency is usually NOT the first property considered for choosing a treatment.
true or false
drug potency is usually the first property considered for choosing a treatment
since a drug can be very potent, but poorly efficacious (response doesn't change, even when dose is increased)
what's the difference between synergism/potentiation versus antagonism?
S/P: antibiotics taken together increase each others' effectiveness (so ADDITIVE effects... ex: 1+1=5)
A: one drug inhibits the other drug taken
a bacteriostatic agent (like tetracycline) and a bactericidal drug (like penicillin) taken together become ________________
(ex: the bactericidal drug requires an actively replicating cell to attack it, but the bacteriostatic drug stops this from happening)
is penicillin bactericidial or bacteriostatic? why?
describe the structure?
-cidal, since it weakens the cell wall
-beta lactam ring with one R group
how does the beta lactam ring work?
what two enzymes does it trigger?
-weakens the cell wall by binding to bacterial Penicillin binding proteins (PBPs)
-thereby, it inhibits transpeptidase (forms polymer bridges to make the cell wall) and activates autolysins (promote cell wall destruction)
____________ enzyme, forms polymer bridges to make the cell wall
__________ enzyme, promotes cell wall destruction
**both are affected upon the binding of ___________
penicillin binding proteins
penicillin G is _______
penicillin V is ________
--is pen G usually narrow or broad spectrum?
IV (or IM)
why is penicillin G IV/IM while penicillin V is oral?
G: unstable in acid, so given IV or IM
V: stable in acid so can be oral, also has a short half life
what are the 2 main organisms that are resistant to penicillin?
how does penicillin usually affect gram positives? gram negatives? anaerobes?
-MRSA and VRE (vancomycin resistant enterococcus)
POS: very good with narrow spectrum penicillins
NEG: good, but need broad spectrum
ANA: very good, but need broad spectrum
Most normal odontogenic infections can be managed
by __________ of the focus of infection (ex: abscesses, lesions) without needing antibiotics.... however if antibiotics are needed, what is usually given?
-amoxicillin (given orally) , or metronidazole, or ampicillin (if needing to take it IV)
true or false
Most odontogenic infections still respond to amoxicillin
what drug should be used in pts who have showed Type I hypersensitivity to the Penicillins?
how do beta-lactamases work?
cleave the beta lactam ring that antibiotics have, so the antibiotic is no longer useful
what is a beta-lactamase inhibitor?
what are some examples
-the bind the beta lactamase and distract it from cleaving the beta lactam ring of the antibiotic
-so this makes the antibiotic more effective
-sulbactam and clavulanic acid
most penicillins excreted via the __________; however ___________ is the exception because it is hepatically cleared (so doesn't require dose adjustment in pts with renal dysfunction)
what is unique about cloxacillin?
this is the only penicillin that isn't excreted via the kidneys
If someone has ever been anaphylactic, don't give them penicillin, instead use an alternative such as _____________
how many penicillins affect:
OC: reduce efficacy of contraceptives
BD: decrease penicillin effectiveness
what do we need to consider if a pt is on an NSAID or Probenecid (a uricosuric agent given to eliminate uric acid from the body) before we prescribe penicillin?
NSAIDs and Probenecid increase penicillin levels, so we don't want them to overdose
penicillin overdose includes: neuromuscular hypersensitivity, agitation, hallucinations, confusion, and seizures.... why?
Penicillin is usually provided as a sodium or potassium salt. So you will need to worry about the counter ion concentration
-the kidneys are the primary organ that eliminates penicillins, so there is very little liver involvement is regulating ion metabolism
why are cephalosporins so similar to penicillins?
how are they different?
-because they have a beta lactam ring too
-however cephalosporins have 2 R groups, rather than just 1
true or false
cephalosporins are similar to penicillins in that they bind the PBPs, however they do not affect transpeptidase or autolysin
what is the main reason for cephalosporin resistance?
-production of β-lactamases called
(this enzyme may even be able to cleave some penicillin β-lactam rings)
cephalosporins are classified as generations, according to when they were discovered (1st-5th)
which generation is most easily destroyed by β-lactamases?
which are the most resistant?
-third through fifth
In general, as you progress from 1st -generation cephalosporins to 5th-generation, there is:
- ________ activity against Gram(-) bacteria
- ________ resistance to destruction by β-lactamases
- _________ ability to reach the CSF
why should 1st and 2nd generation cephalosporins not be used to treat meningitis?
because the higher the generation, the more able it is to cross the CSF
-so 3rd, 4th, or 5th generations should be used instead
most cephalosporins are eliminated through the ________
the exception is __________ which is eliminated by the ________
penicillins and cephalosporins are eliminated via the kidney... what is the exception for each that is eliminated via the liver?
what does probenecid do to penicillins and cephalosporins?
-it increases their toxicity, because it decreases their excretion rate
what may be some side effect from cephalosporins?
-bleeding (impairs vitamin K synthesis)
-may cause buildup of acetaldehyde, causing alcohol intolerance
-may cause calcium deposits in babies
_____ generation cephalosporins may be used as a prophylaxis against infections in surgery patients, if they have mild penicillin allergies
which would be worse to use routinely, a 1st or 3rd generation cephalosporin?
(higher chance of developing resistance)
what generation of cephalosporin is the drug of choice for treating meningitis?
true or false
3rd generation cephalosporins that are used routinely are very likely to lead to C. dif infections
__________ is the only cephalosporin that can treat Pseudomonas aeruginosa
this is a _______ generation cephalosporin
3rd (weirdly enough, 1st, 2nd, 4th and 5th can't treat it, only 3rd)
in general, should you stick to the first and second generation cephalosporin drugs, or the 3rd, 4th, and 5th?
1st and 2nd
___________ is the only cephalosporin that is able to treat MRSA, it is a ______ generation
ceftaroline; 5th gen
are cephalosporins indicated or contraindicated in individuals with a history of severe allergic reaction to penicillins?
-only indicated if the pt has a mild allergy to penicillin
describe a carbapenem
-similar to penicillins and cephalosporins, it has a beta lactam ring, but is mostly used in hospitals for severe infection
-resistant to most beta lactamases
-can penetrate to the CSF
carbapenems are mostly used in hospitals for severe infection
is this a broad or narrow spectrum drug?
what specifically can it kill?
-Pseudomonas aeruginosa and Enterococcus species (not MRSA!)
are carbapenems usually given orally?
what type of cells are they able to target?
no, IV or IM
-gram positive and negative; aerobes and anaerobes
how are carbapenems eliminated?
they must be given with what?
-via the KIDNEY
-cilastatin (a dipeptidase inhibitor, to prevent its degradation) (this is especially true for imipenem, a carbapenem)
what are monbobactams?
what is unique about them?
-monocyclic beta lactams
-only treat gram negatives
-lacks any cross allergy with other beta lactams
____________ kill Pseudomonas aeruginosa
____________ kill Enterococcus species
____________ kill MRSA
____________ kill Salmonella, Shigella
--carbapenems; ceftazidime (a 3rd gen cephalosporin)
--ceftaroline (a 5th gen cephalosporin)
what is the main disadvantage of using Monobactams?
-induces β-lactamase activity
-can be synergistic for renal and oto-toxicity
in order to avoid the potential for the disulfuram reaction to occur, consumption of alcohol would be contraindicated in a patient being treated for acutre necrotizing ulcerative gingivitis with which drug:
trimethoprim exerts its antibacterial effect by acting as a competitive inhibitor of:
b-ribosomal protein synthesis
c-para aminobenzoid acid
grapefruit juice can increase the cardiac toxicity of _______ due to competition for metabolism by CYP3A enzymes
antibiotic prophylaxis is recommended before performing certain dental procedures in high risk patients to prevent:
adverse effects of antibiotic prophylaxis include;
a-induction of resistance gene transfer
b-antibiotic allergy and toxicity
c-selection of antibiotic resistant organisms
e-all of the above
sulfonamide drugs compete with which chemical in the synthesis of folic acid?
advantages of treatment with azithromycin over treatment with erythromycin include:
a-longer half life
b-can be used in dental prophylaxis
c-fewer drug drug interactions
d-less GI upset
e-all of the above
patients should be advised to drink large amounts of water to avoid crystalluria when taking which antibiotics?
what is the drug of choice for treating MRSA?
what class of antimicrobial drugs bind to bacteria ribosomes to cause premature termination of protein synthesis, must be administered either by IV or IM to treat systemic infections, and are associated with risk for nephrotoxicity and/or ototoxicity?
which antibiotic listed below would be considered safe for use in pregnancy?
c-sulfamethoxazole trimethoprim tablet
which class of antibiotics listed below acts to block bacterial DNA synthesis (bactericidal) by inhibiting DNA gyrase (gram negative) or topoisomerase (gram positive) enzymes?
why do we pasteurize milk?
because tuberculosis is often found in cattle and wildlife (usually as M. bovis or M. caprae)
Tuberculosis (TB) is caused by soil bacteria of the Mycobacterium tuberculosis complex, specifically what bacteria?
____% of the world's population carries the TB bacteria, however they're healthy enough that they don't have the active disease
what country has the most TB cases?
when M. tuberculosis reaches the alveoli in the respiratory tract, what are the 2 things that can happen?
-forms a granuloma and causes caseous necrosis --> latent TB
-forms an incomplete granuloma with liquefactive necrosis --> active TB
true or false
If you treat underserved patients, you're at a higher risk to be exposed to TB
Caseous granuloma --> ________ TB
Liquefactive granuloma --> ________ TB
TB gets phagocytosed by the _________ in your alveoli of the lungs
can TB go to other areas of the body other than just the lungs?
yes, TB loves oxygen, so it loves the lungs. ... but it can go to the bones and other areas of the body
__________ TB is the most chronic form of TB
the rate of secondary (re-infection) TB after successful treatment is _______ than the rate of new TB cases
can TB multiply inside of macrophages?
yes, then as the macrophages move throughout the body, the TB can spread
in healthy people, TB infection is usually taken care of with no infection period, however some TB can stay hidden in the _________ and remain quiet/quiescent while the immune system is okay.... then when ____________________, the TB can re-emerge
-the immune system drops
what does it mean to be MDR TB?
(multiple drug resistant)
TB (so you have a positive sputum culture)
and MDR (so resistant to both isoniazad and rifampin)
what drugs are you resistant to with MDR TB ?
isoniazad and rifampin
what does it mean to be XDR TB?
(extra drug resistant)
TB (so you have a positive sputum culture)
and XDR (resistant to isoniazad and rifampin + any fluoroquinolone and at least 3 other second line drugs)
what drugs are you resistant to with XDR TB ?
resistant to isoniazad and rifampin + any fluoroquinolone and at least 3 other second line drugs
what is the difference between primary resistance? and secondary resistance?
PRIMARY: when the person acquired it, the infection was already resistant to a given drug
SECONDARY: the resistance developed during treatment
For ____________ resistant TB strains, the standard Tx takes 2 years and includes injections of painful medications (aminoglycosides) associated with hearing loss and other serious side effects. Tx has significantly poor outcome.
what are the 3 tests that you do to diagnose TB
--TB skin test (testing for interferon gamma release assays)
--if that's positive, then you'll need a chest x-ray
--if that's positive, then you'll need a sputum culture
what is a TB skin test testing for?
interferon gamma release assays (IGRAs)
what does it mean if you have a positive TB skin test?
what does it mean if you have a positive chest x-ray and sputum culture?
-that you at least have latent TB
is TB fast growing or slow growing on an agar plate?
how long does it take to grow colonies?
so how do we normally diagnose TB if someone is getting a sputum culture done?
- VERY slow
- takes 5-18 days
TB bacteria are coated with a ________, which allows them to live inside us and escape removal
true or false
if you're infected with TB you can only expose one other person
false, you can expose thousands (since it's respiratory)
what are some risk factors that increase the likelihood of your latent TB becoming active?
-diabetes (immune system is compromised)
-corticosteroid use (since it's an immunosuppressant)
-living in very crowded areas (high respiratory transmission)
**literally anything that weakens your immune system or makes you breathe in lots of other people's air
if you have latent TB, are you infectious?
how do you treat these pts as a dentist?
-same as everyone else
if you have active TB, are you infectious?
how do you treat these pts as a dentist?
-we can't treat them in a dentist office, the only way they can be treated is if it's in an isolation facility with fitted N95 respirator on the dentist (have to have a respirator, not just a mask)
true or false
the CDC does not recommend routine immunization of health care workers against TB.
however you should have a skin test done before you start work somewhere and again if you ever think you've been exposed to someone with TB
how long does TB treatment usually take?
how long if it's drug resistant TB?
killing the ____________ TB bacilli is the biggest challenge in TB treatment
(because most antibiotics are bacteriocidal, so they need actively growing bacteria, in order to work)
what are the 5 first line drugs for TB?
which of the first line TB drugs can also be used alone for a prophylaxis?
Isoniazid (aka INH)
are you usually just given one first line TB drug? or multiple?
-usually take a combination of 3-4 of them
what is pyridoxine?
another name for vitamin B6
what are some key facts to know about Isoniazid?
-also known as INH
-can be used alone as a TB prophylaxis
-rarely causes hepatitis (reversible)
-causes vitamin B6 deficiency, which can cause neuropathy, so have to take B6 supplements
_____________ causes vitamin B6 deficiency, which can cause neuropathy, so you'll have to take B6 supplements
what is the most useful, and least expensive drug for TB?
hence why it can be given alone as a prophylaxis
what are some key facts to know about Rifampin?
-eliminates dormant TB organisms in macrophages
-can cause jaundice
-can cause renal failure
-turns all body fluids red/orange
what TB drug turns all you body fluids red/orange?
which can cause jaundice?
with TB drug is able to eliminate dormant TB organisms in macrophages?
what are some key facts to know about Ethambutol?
-best tolerated of the first line TB drugs
-can cause optic neuritis (so give pt a vision test)
___________ is given orally and is the best tolerated of the 1st-line drugs.
although ethambutol is safe for kids why may you not want to use it?
because the symptoms of this drug is optic neuritis, so you have to take a vision test to see if you're affected, however kids may not be old enough to do a vision test yet and pass
what first line TB drug may cause an inability to distinguish blue from green?
what are some key facts to know about Pyrazinamide (pza)?
-this is a prodrug, so converts to active form
-inhibits mycolic acid synthesis
-can cause GI upset
-not safe for pregnancy
which of the TB drugs is given as a prodrug?
which of the 5 first line TB drugs are safe for use during pregnancy:
what are the atypical TB drugs?
•Tetracyclines- Minocycline (Dynacin, Minocin)
what is Para-aminosalicylate sodium (Sodium P.A.S.) have to do with TB drugs?
this is bacterioSTATIC against TB
-this is useful because it can stop resistance from occurring (always used in combination with other TB drugs)
what are the 2nd line TB drugs?
"All Can Clear Lungs And Can Ease Respiration"
second-line TB drugs are ________ effective and ________ toxic than the 1st-line drugs but useful in treatment as a mixed regimen and to treat MDR-TB.
what are some key facts to know about Capreomycin?
-works the same as streptomycin, but TB that are resistant to streptomycin are often susceptible to capreomycin
what are some key facts to know about Kanamycin (Kantrex) and amikacin (Amikin)?
-the same as capreomycin (works if streptomycin resistance)
-however, this is more likely to cause renal and neural toxicities
true or false
anything that damages the CN8 is contraindicated for pregnancy
(hence why you shouldn't take streptomycin during pregnancy)
___________ is the most commonly used aminoglycoside (AG) for TB treatment and is very effective and bactericidal.
what are some key facts to know about streptomycin?
-first line TB drug
-most commonly used aminoglycoside
-can cause renal tubular damage, vestibular damage, and ototoxicity
-contraindicated in pregnancy (CN8 damage)
which of the first line TB drugs are able to reach the CSF?
rifampin and isoniazid
most second line TB drugs can be classified as either a _________ or a ____________
what is the newest TB drug that is on the market?
what is the only down side?
Sirturo (made in 2013)
-however this can mess up your heart
traditional TB treatment usually involves which 4 of the 5 first line TB drugs?
why does the treatment of TB patients often include directly observed therapy?
what does this even mean?
-this is when you are being forced to check up on people, because they are of poor compliance, or they're living on the streets and you know they're not likely to keep on top of things
-pts that you know will have a good compliance though can have self administered therapy
when were most first line TB drugs discovered ?
the 1950's and 1960's
what vaccine can be given for TB?
is this given in the US?
why or why not?
-Bacille Calmette Guerin (BCG)
-no, only given to babies in other countries
-it's not really understood how this works, or even if it's effective
critically, preventing and controlling TB infection requires ___ cell immunity.
why may it be beneficial for the BCG vaccine to be given as an IV drug, rather than an IM shot?
with IM, this doesn't go straight to the lungs, so if you're going to produce any memory cells, they won't really be in the lungs
--however if you give it as an IV, it's not affected by the skin, so can go to the lungs easier
(again, the BCG vaccine isn't well understood, which is why it isn't given in America)
the reason the _____ route of BCG vaccine is so effective is that the vaccine travels quickly through the bloodstream to the lungs, the lymph nodes, and the spleen, and it primes the T cells before it gets killed
Currently, ______ TB vaccine candidates are in clinical trials
what 4 drugs inhibit ribosome protein synthesis?
what 3 inhibit cell wall synthesis?
what 2 inhibit nucleic acid synthesis?
what 2 inhibit folic acid synthesis?
-macrolides, aminoglycosides, lincosamides, tetracyclines
-penicillin, cephalosporin, vancomycin
what 2 drugs inhibit folic acid synthesis?
what 2 drugs inhibit nucleic acid synthesis?
what 3 drugs inhibit cell wall synthesis?
what 4 drugs inhibit ribosome protein synthesis?
in general, what are the only reasons that antibiotics should be required?
-signs of severe infection
-signs the infection is spreading
-high risk of possible complications (ex: diabetics or immunocompromised)
usually infections only last a few days, so how long should antibiotics be prescribed for?
how is this different if you're immunocompromised?
-3 to 5 days and revaluate after 2 days (since they usually start to improve within 48 hours)
-you may require an extra 3-5 days after the infection, just to be safe
most orofacial infections typically require ______ days of antibiotic therapy in conjunction with appropriate dental/surgical treatment
what are some ways that the bacteria can increase their antibiotic resistance?
-alter the target on the membrane (so the drug can't bind anymore)
-have enzymes that degrade the drug
-have efflux pumps (drug sent back out of the cell)
-don't have as many porins (drug can't enter)
what is the pathway for folic acid synthesis?
PABA --> (uses enzyme dihydropterate synthetase) --> dihydrofolic acid --> (uses enzyme dihydrofolate reductase) --> tetrafolic acid --> DNA/RNA precursors --> DNA/RNA
what enzymes do sulfonamides and trimethoprims block?
S: dihydropterate synthetase
T: dihydrofolate reductase
how do sulfonamides and trimethoprims inhibit DNA synthesis?
because they inhibit folic acid synthesis, which in turn doesn't allow DNA or RNA to be formed from their precursors
do plants and animals make their own folic acid?
do humans make their own folic acid?
what is the advantage and disadvantage of this?
A: we have to obtain it from dietary sources
D: it's easier for us to have a drug that target it, because we don't naturally have this in all of our cells
what type of inhibitors are sulfonamides and trimethoprim?
why do sulfonamides work so well to block dihydropterate synthetase?
because they are very similar in structure to PABA, and they are a competitive inhibitor against it
Prontosil is a ________ dye that researchers found can be converted into Sulfanilamide which is effective in killing strep pyogenes
in 1937, a drug company made Sulfanilamide Elixir
-they mixed sulfanilamide with glycol and it killed hundreds of people
-this was never tested on animals before it went to market, so after this, Congress created the Food, Drug, and Cosmetic Act which meant you have to prove that something is safe before you can market it
in 1938 Congress enacted Food, Drug, and Cosmetic Act in response to the ________________ poisoning crisis
are sulfonamides bacteriostatic or bacteriocidal?
-they stop the growth of the cells, since they can't make DNA
-plus there's also a lag before the onset of the effect of the drug, because RBCs have a built up storage of folic acid
RBCs have a built up storage of _____________ so this means there may be a lag period before sulfonamides are bacteriostatic
what are sulfonamides mostly used to treat?
-UTIs, ear infections, eye infections, burns (can be a topical)
-can also cross the BBB
what are some ways that bacteria can increase their resistance to sulfonamides?
-more efflux pumps
-make the target enzyme (dihydropterate synthetase) less sensitive
-just make a crap ton of PABA
why would you ever take a combination of two different sulfonamide drugs (ex: sulfamethoxazole and trimethoprim)?
one is slow acting (6-10 hour half life) and the other is long acting (up to 230 hours)
what is an adverse effect of sulfonamides?
-- it's a weak acid with limited water solubility so it can crystallize in kidney
--so drink lots of water
with what drug do you need to make sure that you drink lots of water, so the drug doesn't form crystals in the kidney?
what are the common adverse effects of sulfonamides?
-hemolytic anemia (jaundice in babies)
-Stevens Johnson syndrome (blisters on the skin, from the allergic reaction)
approximately _____% of individuals treated with sulfonamides and/or trimethoprim have some sort of adverse reaction
Stevens Johnson syndrome (blisters on the skin, from the allergic reaction) is due to what drug?
who should not use Sulfonamides?
-pregnant women (since it's a teratogen)
-lactating women (excess bilirubin causes jaundice in babies)
-people with kidney or liver disease (since it's known to crystalize)
if you take PABA supplements, this will interfere with the effectiveness of what drug?
what enzyme does trimethoprim inhibit?
-it has a 100,000 times higher affinity
what is an easy way that something may be resistant to trimethoprim?
if the organism just doesn't have the dihydrofolate reductase enzyme
true or false
sulfonamides and trimethoprims are usually used just one at a time (not in conjunct)
false, they are both usually used together
are sulfonamides and trimethoprims teratogens?
pregnant women obviously need folic acid (hence why they take folate supplements) and both of these drugs are intentionally trying to stop the production of folic acid
what is the main side effect of trimethoprim?
-it's a teratogen and causes neural tube defects
-adverse effects are also more common in AIDS pts
trimethoprim and sulfonamides are synergistic to one another (since they both attack the same pathway, just different enzymes) but what ratio are they used in, when used together?
if a bacteria is sulfonamide resistant, will trimethoprim be effective?
(just because it's resistant to one doesn't mean it's resistant to the other)
what's an easy way to be resistant to sulfonamide?
-have a mutated dihydropteroate synthetase
-the PABA is used to recognizing the mutated enzyme so when the drug comes, it doesn't resemble the enzyme as well so has a harder time being a competitive inhibitor
how does metronidazole work?
-it gets reduced once in the cell and makes active metabolites that damage the cell DNA (so bacteirocidal)
_____________ gets reduced once in the cell and makes active metabolites that damage the cell DNA (so bacteirocidal)
metronidazole is only affective against _________ this includes ____________
red/brown urine may be indicative of _____________
red/orange urine may be indicative of _____________
concurrent use of ______________ and alcohol may result in acute psychosis and the disulfiram reaction (flushing, tachycardia, nausea and vomiting)... so never drink alcohol while taking _____________
between sulfonamides, trimethoprims, and metronidazole, which is more commonly used in dentistry?
how is metronidazole used in dentistry ?
400mg three times a day, for 5 days
treats NG and periodontitis
what are the 3 components of triple antibiotic paste (TAP)?
-metronidazole, minocycline, ciprofloxacin
___________ drug is often used in dentistry, 400mg three times a day for 5 days, and is used to treat necrotizing gingivitis and periodontitis
which is more likely to attack aerobes? anaerobes?
M: only does anaerobes
how do quinolones work?
they block DNA synthesis either by inhibiting DNA gyrase (in gram -) or topoisomerase (gram +)
what enzymes does quinolones block if gram - cells? gram +?
NEG: DNA gyrase
_________ blocks DNA synthesis either by inhibiting DNA gyrase (in gram -) or topoisomerase (gram +)
there are four generations in quinolones, name 2 second gen and 1 third gen?
SECOND: ciprofloxacin (used in triple antibiotic paste), levofloxacin
for fluoroquinolones, what are they really good at killing?
true or false
some organisms may be more sensitive to one generation of fluoroquinolones than others)
(hence why there's 4 generations)
what drug family is organized into 4 generations along with 4 groups?
what do the groups signify?
1: for UTIs
2: broad spectrum
3: gram positives
4: gram positives
what are some side effects of fluoroquinolones?
CNS toxicity and Cardiac changes
Tendonitis and cartilage damage! (so don't give to pregnant women, kids that are still growing, or elderly)... this is the Black Box warning
the "black box warning" for ___________ includes tendonitis and cartilage damage, so you should never give to anyone who's growing (aka: kids (<16) or pregnant women)
are quinolones safe in pregnant women?
no, can cause tendonitis and cartilage damage
what two things increase the toxicity of fluoroquinolones?
NSAIDS and antacids (polyvalent cations)
how do tetracyclines work?
work on gram negative cells, since requires two membranes
-passively diffuses through first membrane, but then needs energy to actively transport through inner membrane
-it then binds the rRNA so that tRNA can't bind (so no proteins can be made)
what drug requires passive transport to get through the outer membrane of gram negative cells, but needs active transport to get through the inner membrane?
what is the main reasons that people use tetracylcines?
-they're very broad
-mostly used for acne and rosacea though
you shouldn't take antacids with ________ or ____________
can tetracyclines affect the CNS?
mostly just used for acne and rosacea
what drug can cause dental enamel staining and hypoplasia?
the main side effect of tetracycline is ______________
the main side effect of minocycline is ______________
do we use tetracyclines in dentistry?
although they are maybe able to treat some chronic periodontitis, they will cause severe stains on the teeth
-so if you're desperate, and the perio is severe, you can use it (risks vs benefits)
why does tetracycline stain teeth?
does it stain bone?
-it chelates in the teeth
-yes, but the bone remodels over time, so eventually the stain will go away, but teeth don't remodel so the stain will remain in the teeth
tetracycline should not be used in children less than ______ years of age
(then once the teeth are all done forming, it's okay to use)
if an adult has severe periodontitis, you may be able to use _________ as an adjunct to SRP
how is this used?
-Periostat (a doxyclince taken BID)
-the drug is put directly into the sulcus, so you can't brush or floss for 7 days... only able to use mouthwash
with __________, the drug is put directly into the sulcus, so you can't brush or floss for 7 days... only able to use mouthwash
(the specific brand of drug is called Atridox)
Atridox™ meets the standard of being a "stand alone" therapy for periodontitis. A "stand alone therapy" for periodontitis is defined as any therapy that is at least 75% as effective as scaling and root planing.... Atridox is a type of _____________
Arestin™ is a minocycline that comes in the shape of little beads that you can put directly into the sulcus to aid in perio pts
can this still cause tooth discoloration though?
Minocycline stains teeth differently than tetracycline and doxycycline.
Tetracyclines stain teeth through their ability to form a complex (chelation) with __________; complex is preferential deposited in dentine and to lesser extent enamel.
how does minocycline stain teeth?
we're not really sure, but there's three theories:
INTRINSIC: binds to collagen fibrils in teeth
EXTRINSIC: etches onto the enamel
CHELATION: chelates with iron; deposits in teeth
state whether each is bactericidal or bacteristatic:
state broadly what each does
M: inhibit DNA synthesis
A: inhibit protein synthesis
S: inhibits folic acid
T: inhibits folic acid
M: inhibit protein synthesis
C: inhibit cell wall
P: inhibit cell wall
L: inhibit protein synthesis
T: inhibit protein synthesis
F: inhibit DNA synthesis
V: inhibit cell wall
true or false
macrolides are very small in their structure
false, they're pretty big drugs
how do macrolides work?
what are the 2 most common macrolides
-inhibit protein synthesis by binding rRNA
-erythromycin and azithromycin
why must you take macrolides on an empty stomach?
what is the exception?
-to make them more available?
-erythromycin (has to be taken on an full stomach, that way the gastric acid is occupied and won't attack it... it's too sensitive for attack)
what drug must you always take on an empty stomach?
-macrolides (except erythromycin)
________ is supplied in a protected tablet or capsule since it is inactivated by stomach acid
(and it's also recommended to take with food, so the gastric acid doesn't attack as harshly)
if a pt is allergic to penicillin, would macrolides be a good choice?
are macrolides more affective against gram positive or negative?
Diarrhea and GI distress due to stimulation of motilin receptor, is seen with what drug?
(think GI distress.. this drug is taken on an empty stomach)
_____________ interferes with P450 metabolism of several drugs, so this can lead to heart arrhythmias
inhibitors of CYP3A increase the cardiac toxicity of _______________, which is why you should not drink grapefruit juice when you're taking this drug
is erythromycin likely to have lots of drug drug interactions?
because it interferes with P450 (which is useful in tons of drug metabolism reactions)
what are 2 drugs we know that are prodrugs?
Pyrazinamide (1st line TB drug)
Dirithromycin (a macrolide)
lots of macrolides cause drug drug interactions because they involve the enzymes of the liver (P450).... which two do not affect the liver (and therefore may be an advantage, because there's less drug drug interaction)?
what is the advantages with Azithromycin and Dirithromycin?
neither type of Macrolide affects the liver microsomes... which means both are less likely to cause drug drug interactions (this is an advantage over erythromycin and clarithromycin)
which macrolides are most likely to be used in a dental prophylaxis?
what is special about clarithromycin and azithromycin?
these are the 2 macrolides that are able to be used in a prophylaxis
out of the 4 (erythromycin, clarithromycin, azithromycin, dirithromycin):
-causes GI upset?
-causes drug drug interactions?
-able to cause jaundice?
-used in prophylaxis?
why is Dirithromycin not used as a dental prophylaxis?
-because it's a prodrug, and it's not highly bioavailable (so if you gave this one hour prior to an appointment, it wouldn't have enough time to become active and reach the site of possible infection)
what are the only two lincosamides?
clindamycin and lincomycin (they're the exact same, except for one atom)
how do lincosamides work?
-Bind the ribosomal subunit and inhibit protein synthesis (so bacteriostatic)
are lincosamides (clindamycin and lincomycin) good for beta lactam allergies?
___________ is able to concentrate in neutrophils and macrophages (which then migrate to the site of infection, bringing the drug)... sweet!
____________ affects bacteria in gut for up to 2 weeks after last dose
lincosamides (clindamycin and lincomycin)
what is the major adverse effect of Clindamycin?
-major concern is antibiotic-induced diarrhea and colitis, esp. pseudomembranous colitis often due to C. dif
why antibiotic is likely to cause C. dif as an adverse effect?
how do you treat this?
-just stop taking the drug (switch to a different class of antibiotics)
what are aminoglycosides
-inhibit protein synthesis by binding rRNA
-only effective against aerobes
-can't be given orally, have to be IM
what are the 2 unique things about aminoglycosides?
-can't be given orally (has to be IM, since it's not absorbed in the gut)
-only affects aerobes
name a drug that has to be given IM and can't be given orally?
(so we don't really ever use these in dentistry)
what are the 2 main side effects with aminoglycosides?
(since the drug concentrates in the kidneys and the ears)
since aminoglycosides can cause ototoxicity (hearing and balancing problems) , what can you do to reduce this chance?
-only give the drug once a day (may make it less toxic)
what does vancomycin do?
is it bacteriostatic or cidal?
-inhibits cell wall synthesis by binding transglycosylase enzyme (needed for synthesis)
___________ inhibits cell wall synthesis by binding transglycosylase enzyme (needed for synthesis)
what can Vancomycin kill?
how is vancomycin given?
-it doesn't absorb from the GI to systemic circulation, so it's not given orally (unless you're specifically trying to target the GI (ex. in C dif)).
how would you give Vancomycin for killing MRSA? killing C dif?
(oral or IV)
MRSA: IV (since the drug won't diffuse from the GI tract to the systemic circulation, so it has to be IV)
C dif: oral (since it won't diffuse, so it will concentrate in the GI tract, where C dif is)
red man syndrome is a hypersensitivity reaction to ______________
in an antibiotic prophylaxis, the loading dose should be ______ times the maintenance dose
(that way it's already at high concentration at the target site when the surgery starts)
what are the adverse effects of giving an antibiotic prophylaxis?
-creates resistant infections
-encourages resistant gene transfer
when should you take an antibiotic prophylaxis?
who does the American Heart Assocaition say should have an prophy?
-30 to 60 minutes before treatment
-pts with: pre-existing cardiac conditions, cardiac transplant recipients, or individuals with prosthetic cardiac devices
microorganism attaches to surface of heart valve and forms a vegetative growth... this is called ____________
(what we're trying to prevent by using an antibiotic prophylaxis)
What is the most common indication for use of trimethoprim-sulfamethoxizole?
primarily UTIs (also used for ear, respiratory, and GI infections.)
What is the mechanism of action of metronidazole? What enzymatic reaction is required for it to be effective?
active metabolites damage bacterial DNA: reduction of nitro group
Metronidazole is used to treat which parasitic diseases?
trichomoniasis, amebiasis, giardiasis
What are some of the adverse side effects of metronidazole therapy?
metallic taste, reddish-brown urine, GI effects, neuropathy
The fluoroquinolones are derivatives of ...?
they are C6 derivatives of nalidixic acid
What is a pharmacokinetic advantage of some of the newer generation fluoroquinolones?
broader anti-bacterial spectrum; longer half-life
6. Why would the use of Sparfloxacin (a flouorquinolone) be contraindicated in a patient with a history of cardiac arrhythmia?
↑ risk for cardiac conduction changes (prolonged QT syndrome)
-Drug-drug interactions between what group of common OTC meds and fluoroquinolones has the potential for increased CNS toxicity?
-What OTC preparation inhibits absorption of fluoroquinolones?
-NSAIDs increase CNS toxicity of fluoroquinolones
-antacids; polyvalent cations inhibit absorption
what OTC preparation can block oral absorption of tetracyclines?
What oral tetracycline can be given twice a day as an adjunct following SRP to treat adult periodontitis?
When combined with a bioabsorbable polymer, what tetracycline forms an extended-release gel that can be placed in the subgingival periodontal pocket to treat chronic adult periodontitis?
How long does this gel preparation continue to release high concentrations of drug?
what is a 'stand-alone' therapy for periodontitis?
any therapy that is at least 75% as effective as scaling and root planning (SRP)
(ex: doxycycline combined with a bioabsorbale polymer)
What tetracycline antibiotic comes in a microsphere formulation that is placed in the subgingival pocket as a powder and upon contact with crevicular fluid adheres to pocket surfaces to form a 14-day extended-release product for use in combination with SRP to reduce pocket depth in adults with periodontitis?
what are the 2 disadvantages of Triple Antibiotic Paste?
-possible staining (minocycline)
-paste binds to dentinal structures, making removal of paste challenging
minocycline can stain either via: intrinsic theory, extrinsic theory, or by chelation of ________
__________ bind rRNA, inhibit elongation of bacterial protein by peptidyltransferase
What is the route of administration for erythromycin lactobionate?
What macrolide is effective in management of acute periapical abscesses?
grapefruit juice inhibits _________ enzymes which also metabolize _____________
(so this causes erythromycin to be toxic)
High doses of macrolides can cause what transient condition?
transient auditory impairment; temporary hearing loss
lincosamides are useful in treating certain oral bacterial infections caused by microorganisms that are resistant to what group of antibiotics? Why is clindamycin particularly useful for treating abscesses?
useful in treating infections against microbes resistant to β-lactams (use in place of amoxicillin or Pen V); useful in treating abscesses because drug concentrates in neutrophils and macrophages that seek the site of infection by chemotaxis
Why are aminoglycosides ineffective against anaerobic organisms?
aminoglycoside transport across the bacterial inner membrane requires aerobic conditions
Which aminoglycoside is most commonly used in a topical preparation?
how does each work, when they bind the rRNA?
M: inhibit elongation of bacterial protein by peptidyltransferase
A: cause premature termination of bacteria protein synthesis
L: inhibit microbial protein synthesis
T: disrupt tRNA-mRNA interaction
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