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213 Cards in this Set

  • Front
  • Back
Characteristics of tumor cells (5)?
1.derive from our cells (normal)
2. Aberrant (abnormal)
3. Clonal (from 1 cell)
4. Hyperproliferative: no controls
5. Can be metastatic
Cancer is ___highest cause of death?

what % of people develop cancer?
second

30%
etiology for cancer?

contributing factors?
80% unknown.

viruses, environmental, radiation, life style
what percentage of tumors has tx been effective on mortality?
less than 20%
Grade vs stage?
Grade: histology (biopsy) or blood smear
stage: whole organ level (single mass or metastasis)
failure of chemotherapy usually do to ?
80% due to resistance
types of chemotherapy resistance?
single agent: resist build to only 1 agent
multidrug resist: to many
Combination chemo is based on?
side effects of drugs (most are myelosuppressive at 28 days so cycle 1 month)
Why do combination chemo?
overcome resistance
enhance anti-tumor effect
rescue normal cells
CR for chemo is? PR?
Complete response: no disease left
Partial: greater than 50% size reduction
what are teh 3 major classes of chemotherapeutic agents?
1. Alkylating agents
2.Antimetabolites
3 Plant alkaloids
Alkylating agents do?
bind covalenty to dna (stop cell growth)
alkylating agents derived from?
chemical war fare agents
alkylating agents exs?
Cyclophosphamide
carmustine
Antimetabolites do?
block biosynthesis/use of cellular metabolites
how do antimetabolites differ from alkylating agents?
better for slower growing tumors
exs of antimetabolites ?
methotrexate and 5-fluorouracil
Plant alkaloids exs?
vincas: vinblasting, vinorelbine, vindesine
taxenes
how do the vincas work?
arrest cell division by stoping mitotic spindle
how do taxenes work?
stabilize microtubules to inhibit mitotic spindle assembly (stop cell division)
what are the 3 major toxicities of chemotherapeutic agents?
1. myelosuppression (bone marrow)
2. dermatologic
3. GI
dose limiting is due to
myelosuppression (b/c makes pts susceptible to infections
Dermatologic toxicity ex is?
alopecia (hair loss)
2. extravasation necrosis: if administered outside vein, tissue dies
3. oral mucositis
how treat oral mucosits?
saline/bicarbonate rinse
2. mucosal coating
3. lubricating agents
topical anesthetics
5. film forming agents
types of nausea and vomiting? time/cause?
acute: within minutes of drug injection
chronic: hours/days
anticipatory: smells, colors, places, etc.
subdivisions of chemotherapeutic agents are?
anti cancer and anti infective
disinfectant vs antiseptic?
dis: remove microbes
anti: skin use
Selective toxicity is? is related to?
harms only invading microbe

mechanism of action
drugs that attack cell walls?
penecillin
cephalosporins
vancomycin
drugs that attack protein synthesi/
macrolides
tetracycline
clindamycin
drugs that destroy cell membrane function?
fungal membranes: polyene, azole
altered nucleic acid synthesis?
fluoroquinolones
sulfonamides and trimethoprim (thymidine synthesis)
metronidazole does?
is metabolized by anaerobic bacteria or amebas (metabolite kills organism)
antibiotic-associated colitis is ex of?
overgrowth of non-susceptible organisms
antibacterial spectrum is?
type of bacteria that a drug is usually effective against
extended spectrum drugs means?
intermediate between narrow spectrum and broad spectrum
exs of narrow spectrum antibiotics?
Extended?
broad?
pen g and v
amoxicillin and cephalexin
tetracyclines, sulfonamides, ciprofloxacin
drugs for anaerobic bacteria
clindamycin and metronidazole
exs of problem bacteria?

what does "problem" mean?
m. tuberculosis
s. aureus
pseudomonas aeruginosa

resist normal antibiotics
MIC is?
minimum inhibitory concentration: amount to achieve inhibition
what are the drug types that inhibit cell wall synthesis?
Pens, cephalosporins, (Beta lactam antibiotics)
what is clavulanic acid?
a beta lactamase inhibitor given with amoxicillin to increase its effectiveness
Macrolide antibiotics do? first drug of this type was?
inhibit 50 s ribosome

erythromycin
are they broad or narrow spectrum?
extended spectrum
Most widely used macrolide?

another ex?
azithromycin

clarithromycin
Tetracyclines MOA?

ex?
inhibit bacterial protein synthesis (30 s)

dyxycycline
adverse effects of tetracyclines?
high concentrations in skin and salive
deposite with Ca in teeth and bones.
tetracycline absorption can be prevented by?
dairy, antacids
MOA of fluoroquinolones?

cidal or static?
altered nucleic acid metabolism (inhibit DNA gyrase) (bacterialcidal)
Ex of fluoroquinolones?
ciprofloxacin, levofloxacin (improved against gram+)
MOA of Sulfonamides and trimethoprim?
inhibit bacterial folic acid synthesis and recycling
why is trimethoprim included?
adminstered with sulfamethoxazole (effects the same pathway)
Why fungi are important even though not as common?
b/c candida is 4th most common cause of hospital-acquired bloodstream infections
most common fungal pathogens effecting humans?
A. fumigatus
C. albicans
C. glabrata, parasilosis, tropicalis, krusei,
cryptococcus neoformans
Fungal drugs discussed? MOA?
amphotericin B: binds ergosterol (in cell wall)
Azoles: inhibit ergosterol biosynthesis
downside to amphotericin B?
IV, side effects: kidney
ex of azole ?
fluconazole (oral med)
how do antivirals usually work?
attack early stages of viral DNA replication with antiviral nucleoside analogs
ex. of antivirals?
acyclovir: herpes
Zidovudine: reverse transcriptase inhibitors
most common antiparasitic drug?
metronidazole
gut parasites?

intestinal parasite common in USA?
round/flat worms

pinworm
drugs for malaria?
chloroquine
Mefloquine (for chloroquine resistant strains)
some sulfa drugs (folic acid inhibition)
what are the types of oral infections?
1. chronic
2. Chronic-subacute with acute exacerbations
3. Intensely acute
ex. of chronic infection?
periodontisis
ex of chronic-subacute infections?
percoronitis, periodontal abscess
ex of intensely acute infections?
necrotizing gingivitis, pa abscess, cellulitis,
how many microbes usually in orofacial infections?
2-8 (polymicrobial)
why do orofacial pathogens become pathogenic?
local variables change
orofacial infections have ___ onset?

can usually be treated with?
rapid (so quick cure too)

incision and drainage (not antibiotics)
why not just use antibiotics instead of incision and drainage?
1. antibiotics do not diffuse well in infected areas
2. inactive antibiotics by pH
3. abscess microbes not alwasy dividing (low metabolic state)
4. high levels of antibiotic inhibitors
periodontal abscesses are due to
breakdown of periodontum within gingival wall of pocket (purulence accumulation)
predominant microflora in periodontal abscess?
74% anaerobes
67% gram - rods
what are the beta lactam antibiotics reserved for hospital aquired infections (serious ones)
cabapenems, monobactams
penicillins effect better gram ___?

what % of bacteria from mouth are sensitive to one of the penicillins?
+.

90%
Pen G is good b/c?

downside?
most active form

narrow spectrum, not stable in acid (not orally admin), short half life
how overcome short half life of Pen g?
Procain and benzathine pen G are insoluble salts. IM injection
what is Pen V?
same as G, but stable in acid
Penicillinase-resistant Penicillins aka?

exs?
anti-staphylococcal penicillins

best is Dicloxacillin for oral
cloxacillin, oxacillin, nafcillin, methicillin
penicillinase resistant pens are ___spectrum?
narrow
exs of extended spectrum penicillins?

which is prototype and which is better taken orally?
ampicillin and amoxicillin

ampicillin
broad spectrum penicillins exs?
piperacillin and mezlocillin. not used b/c not orally effective
beta-lactamase inhibitors exs?
clavulanic acid
what are the initial drugs of choice in orofacial infections?
Pen V and amoxicillin
when use parental pen G?
sever infection
oral route compromised
how do pen allergies manifest?
maculopapular or urticarial skin reactions
which types of allergic reactions are most life threatening?
immediate: seconds to 1 hour after exposure
what is an accelerated allergic reaction?
urticaria and angioedema 1-72 hrs post exposure
most common cause of antibiotic induced diarrhea/colitis?
amoxicillin
NSAIDS and penicillins? and probenecid?
both increase half life of penicillins by decreasing renal excretion
what is different about cephalosporins?
more diverse group (2 spots for substitutions)
how are cephalosporins grouped?
4 generations
first generation cephalosporins are?
exs or oral and parenteral drugs?
older, extended spectrum antibiotics
oral: cephalexin
Parenteral: cefazolin
uses of first generation cephalosporins?
tx staphlococcal and streptococcal infections
surgical and endocarditis prophylaxis
how do 2nd generation cephalosporins differ from 1st?
more stable against beta lactamases (thus increased activity)
major use of 2nd gen cephalosporins?
tx respiratory infections
third generation cephalosporins are ___ spectrum?
differ by?
broad

used against gram - (improbed antibacterial effects), resistant to most beta lactamases
3rd generation cephalosporins used for?
serious gram - infections
meningitis, pneumonia, gonorrhea, sepsis
4th generation cephalosporins differ by?

ex?
more resistant to beta lactamases, more active against gram + bacteria.

cefepime
cephalosporins uses in dentistry?
against orofacial pathogens but not oral anaerobes
cephalosporins adverse effects?
cross allergy with penicillins (rare that is serious or has anaphylaxis)
drug interactions of cephalosporins?
antacids decrease plama concentration
ex of carbapenems?
meropenem, ertapenem, imipenem (ME I)
carbapenems ___ spectrum?
beta lactamases effect by?
pregnancy rating?
wide
not hydrolyzed by most
b or c
carbapenems can raise serum levels of ?

can cause?
liver transaminases

colitis, skin rash
first carbapenem?
imipenim/cilastatin
imipenem is metabolized in?
kidney (but found to be toxic to kidney)
why are meropenem and ertapenem not administered with cilistatin?
not nephrotoxic
ex of monobactams?
aztreonam
aztreonam spectrum?
narrow (gram -)
drugs used if oral infection is mix of gram + and -?
amoxicillin or ampicillin (if beta lactamase producer, add in clavulanic acid)
most important glycopeptide antibiotic?

does?
vancomycin

cell wall inhibition
vancomycin spectrum?
narrow, gram +
uses of vancomycin?
for resistant strains
vancomycin is given?
IV (not well absorbed)
adverse effects of vancomycin are?
pain at injection site, histamine release (from high blood levels), nephrotoxicity
ototoxicity, skin rash (red man syndrome)
what drugs bind the 50s subunite?
macrolides, lincomycin, clindamycin, chloramphenicol
exs of macrolides?

aka?
erythromycin, clarithromycin, azithromycin

large ring antibiotics
are macrolides cidal or static
spectrum?
static

extended (effective especially for gram +)
absorption of macrolides?
via salts derivatives b/c by themselves are not acid stable
adverse effects of erythromycin?
10-20% get GI symptoms
reversible liver injury (occasionally)
Deafness
torsades de points (long QT interval) arrythmias
metabolized in liver, drug interactions (inhibits their metabolism)
how does clarithromycin differ from erythromycin?
same spectrum,
longer half life, acid stability, better absorption
Azithromycin differs b/c has ?

how differ?
additional nitrogen atom in ring

spectrum includes more gram - than erythromycin
azithromycin distribution?
more in tissues very quickly so little in blood (so longer half life,68 hrs)
macrolides in dentistry?
against acute orofacial infections (if beta lactam allergy)
not good against gram -
endocarditis (clari, azithromycin)
most common mechanism of bacterial resistance for macrolides?
erythromycin resistant methylase:
when take erythromycin?
1 hr before
2 hrs after meal
what is done to macrolides to increase absorption?
salts, enteric coating
erythro and clarithro and azithro excreted by?
urine
azi: bile
max adult does of macrolides?
if renal impaired?
4g/day
1.5g/day
macrolide drug interactions?
inhibit metabolism of other drugs
can decrease cardiac glycoside metabolism
if co administration with oral contraceptive, can increase hepatic cholestasis likelihood
contraindications of macrolides?
pts with allergies
pts with history of cholestatic hepatitis
pts taking other drugs that together can lead to torsades de pointe
exs of lincosamides?
lincomycin and clindamycin
clindamycin differs from loncomycin by?
is chlorinated, giving increased antimicrobial potency and better absorption from GI
lincosamides spectrum
narrow: gram + but good against anaerobes (static)
lincosamides metabolized in?
excreted in?
taken via?
liver
biles and urine
oral
adverse effects of lincosamides?
may mild GI
metallic taste sensation
clindamycin is drug most often associated with ?
antibiotic associated colitis
contraindications for lincosamides?
do not co administer with neuromuscular blocking drugs
dental indications for clindamycin?
purulent osteitis (bacteroides infections)
if conditions do not respond to other drugs
prophylaxis in pts allergic to pen
Tetracyclines effect?
30s ribosome subunit
what do the tetracycline derivatives differ by?
duration/rate of excretion/metabolism
tetracycline derivatives:
short acting
medium
long acting?
short: tetracycline
Med: methacycline
long: doxycycline
tetracycline spectrum?

static of cidal?
broad (includes rickettsia)

static?
used for?
tx of serious nosocmial infections for highly resitant strains (although there are resistant forms of tetracycline)
maleria
tetracycline distribution?
high in skin and saliva, well distributed
can deposite in developing teeth and bones
absorption of tetracycline? % absorbed?

prevented by?
incompletely absorbed (doxy better)
tetra: 60-80
doxy: 95-100%

dairy, antacids
tetracyclines metabolized by? excreted by?
met: liver
exc: kidney
Adverse reaction and contraindications to tetracyclines?
C. albicans superinfections,
phototoxicity
GI difficulties
do not take before 8
pregnancy (preg D)/breast feeding
drug interactions for tetracyclines?
reduce efficacy of cell wall inhibitors
reduce insulin requirements
increase serum blood levels of digoxin
increase coumarin effects
tetracyclines used in dentistry for?
alternative to pens,
acute necrotizing ulcerative gingivitis,
perio disease
aminoglycosides act on?

static or cidal?
30s subunit (some act on both)

cidal
ex of an aminoglycoside?
gentamicin
Gentamicin is used for?
serious infections by gram -s.
gentamicin spectrum?
extended
absorption of aminoglocosides?
excretion?
not orally
in urine
adveres effects of aminoglycosides?
8th CN toxicity, (hearing and vestibular function of innner ear)
toxic to kidney
chlorampheniol does?
inhibits bacterial protein synthesis
first discovered!
absorption of chloramphenicol?
complete orally and crosses BBB (use for meningitis)
why is chloramphenicol not used?
anemia, "grey baby syndrome",
not used in orofacial infections
mupirocin is a ?

used for?
topical antibiotic that inhibits Bacterial RNA/protein synthesis.
impetigo, or nasal cavity to control staph infections
streptogramins are like/do?
macrolides (block protein synthesis
oxazolidinones are?
newest
classes of drugs that inhibit bacterial NA sythesis?
Quinolones
Sulfonamides and trimethoprim
Quinolones exs?
older ones for UTI: nalidixic acid, cinoxacin
Fluoroquinolones; ciprofloxacin, levofloxacin
what do fluoroquinolones do?
inhibit dna gyrase.
how does levofloxacin differ from ciprofloxacin?
improved against gram+
quinolones spectrum?
gen 1: limited
gen 2: broad spectrum
gen 3: better when broader spectrum needed
gen 4: broad, plus anaerobes
absorption of quinolones?
half-life?
excretion?
good orally
long half-lives (gen 3,4)
kidneys
Adverse effects of quinolones?
mild. cartilage damage if growing (do not take under 18 yrs)
intereacts with antacids, phototoxicity, arrythmias,
sulfonamides are derived from ?
p-aminobenenesulfonamide
solubility of sulfonamides?
low, especially in low pH (they are weak acids)
how do sulfonamides work
inhibit dihydropteroate synthetase (stop folic acid synthesis)
trimethoprim does?
inhibits step in folic acid synthesis
what does folic acid do?
used for synthesis step in nucleotide synthesis
sulfonamides used to tx?
respiratory, urinary and GI infections
(nothing orally)
absorption of sulfonamides?
metabolized by?
excreted by?
penetrate CNS !
liver
kidney
side effects of sulfonamides?
GI problems:8%
3-5% skin rash
drug interactions of sulfonamides?
can increase oral anticoagulants
stuff with PABA (sunscreens, health foods) contraindicated
how does metronidazole work?
metabolized by bacteroides to products that damage NA
(also for protozoans)
if someone is at rist for mycobacterial infection, first step is?
prophylaxis, preventative
first line anti-tubicular drugs (less toxic) ex?
isoniazid
Isoniazid is used for?
prophylaxis and tx
isoniazid does?
inhigits synthesis of mycolic acids in cell wall, bactericidal (only against active bacteria)
side effects?
older pts: hepatic damage
nervous system toxicity (prevent by b6 vitamin)
second line antitubicular drugs?

aka?
capreomycin and cycloserine

retreatment agents
downsides to capreomycin and cycloserine?
cap: injection
cyclo:1% of pts psychosis (must be monitored for CNS effects)
what is MAC?

what is it?
mycobacterium avium complex

for pts with AIDS, is clarithromycin, or azithromycind plus rifabutin to treat tb infection by m. avium
what heart conditions warrant prophylaxis for IE?
Prosthetic valve, previous IE, congential heart disease (CHD), repaired heart with prosthetic material/devise, repaired CHD with residual defects, transplants with valvulopathy
malaria is caused by?

most dangerous cause?
4 species of plasmodia

p. falciparum
how get malaria/ stages?
infected bite: sporozoites into blood-->liver-->tissue schizont which then rupture and merozoites enter circulation enter erythrocytes and begin cycle again
antimalarial drugs active against?

aka?
erythrocytic forms

schizontocides
what does malaria rely on in humans?
proteins form erythrocytes. (this is what the schizontocides probably interfiere with
how does the accumulation of p. falciparum and p. malariae differ from ovale and vivax?
falciparum and malariae leave no residual merozoites in the liver and thus cannot have recurrent episodes later on
what is the drug of choice to tx liver for malaria?
primaquine
drug to tx malaria in the blood?
chloroquine
chloroquine absorptions?

excreted by? half life?
good orally. accumulates in liver

kidneys. 7 days
side effects of chloroquine?
at prophylaxis levels, none.
dizzy, headache, GI upset/vomit, skin rashes, itching and blurring of vision
at high doses, can cause retinopathy *bulls eye), lupus like skin, cardiovascular toxicity
chloroquine effects on body tissues?
relaxes smooth muscle, antiarrhythmic, antiinflammatory action
what is the chloroquine drug that is save during pregnancy?
chloroquine phosphate
Mefloquine is for?

half life?
strains of P. falciparum ( a single dose can be curative)

14 days (efective levels for up to 30 days)
mefloquine side effects?
GI upset, sometimes serious psychiatric effects
quinine is used for?

absorption? half life?
erythrocytic forms

orally (half life of less than 5 hours)
quinine as IV?
can be, but hazardous due to cardiotoxid effects,
toxicity with quinine causes?
cinchonism: headache, etc
atovaquone is good as a ?
blood schizotocide: inhibits electron transport
Proquanil does?
inhibits plasmodial dihydrofolate reductaase activity
what is artimesinin for?
erythrocitic stages of P. vivax/falciparum
Halofantrine is for?
blood schizontocide (alternative to quinine)
what are the antimarlarials for exoerythrocytic forms (outside blood)?
(kill liver forms)
primaquine, pyrimethamine, sulfonamides, tetracyclines
What is the prototype of the 8-aminoquinoline compouds?
primaquine
Primaquine absorption?
rapidly absorbed orally and then rapidly converted to quinone
primaquine does?
interfere with ubiquinone in mitochondria
downside to primaquine?
hemolytic anemia, methemoglobinemia (with persons with glucose 6 p dehydrogenase deficiencies)