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IBI Test 2 > B3.022 Las Drogas > Flashcards

B3.022 Las Drogas Flashcards

(153 cards)

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1
Q

how do inhibitors of cell wall synthesis work?

A

B-lactams and vancomycin block enzymatic steps outside of the cell or in the periplasmic space
other ICWS act at intracellular sites

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2
Q

general workings of penicillin

A

very selective toxicity (high chemotherapeutic index)
bactericidal in growing, proliferating cells
primarily used for gram +

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3
Q

mechanism of action of penicillin

A
  1. covalent binding to transpeptidases/penicillin binding proteins
  2. inhibition of transpeptidase reaction (cross linking of cell wall)
  3. activation of murein hydrolases (autolysins)
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4
Q

penicillin absorption

A

oral
acid-sensitive
can also be parenteral (IV, IM)

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5
Q

penicillin distribution

A

good to most tissues and fluids

poor penetration into eye, prostate and CNS

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6
Q

penicillin metabolism

A

variable

not usually significant

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7
Q

penicillin excretion

A

excretes by tubular secretion (organic acid secretory system)
EXCEPTION: nafcillin in bile
oxa-,cloxa- in urine and bile
short half life

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8
Q

which drugs exhibit time dependent killing

A

pens
cephs
vancomycin
time above MBC relates to efficacy

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9
Q

pen G

pen V

A

primarily useful against gram +

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10
Q

anti staph penicllins

A 
nafcillin
methicillin
oxacillin
cloxacillin
B lactamase resistant
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11
Q

extended spectrum penicillins

A 
ampicillin
amoxicillin
ticarcillin
piperacillin
mezlocillin
extended gram - activity
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12
Q

anti-psuedomonal penicilins

A

ticarcillin
piperacillin
mezlocillin
effective against proteus, pseudomonas

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13
Q

problem w anti-pseudomonal penicillins

A

rapid emergence of resistance
use in combo w aminoglycosides or fluoroquinolones
POWERFUL: use only when indicated, protect therapeutic value

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14
Q

ampicillin rash

A

10% incidence
90% for mononucleosis patients
self limiting, often does not recur

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15
Q

hypersensitivity reaction of penicillins

A 
major adverse effect
10-15% claim allergy
complete cross reactivity
not dependent on dose
rapid onset
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16
Q

other adverse effects of penicillins

A

seizures induced by high doses

particularly in renal failure

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17
Q

3 primary resistance mechanisms to penicillin

A
  1. no cell wall, no activation of murein hydrolases, metabolically inactive
  2. inaccessible PBPs
    - gram neg
    - MRSA
  3. B lactamase production
    - plasmid mediated
    - either use B lactamase resistance pens or co administer B lactamase inhibitor
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18
Q

problems associated with penicillin use/overuse

A

sensitization
selection for resistant strains
superinfections by resistant organisms

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19
Q

general overview of cephalosporins in comparison to penicillin

A

structure and function similar to penicillins
less sensitive to B lactamases
broader spectrum of activity
some cross reactivity w pen-sensitive patients
more expensive than pens

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20
Q

absorption of cephs

A

poor oral

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21
Q

toxicity of cephs

A

more toxic than pens

particularly renal

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22
Q

should you use a pen or ceph?

A

if a pen will work, use it

cephs secondary ICWS

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23
Q

describe the ceph classification system

A 
1, 2, 3, 4 generation
chronology of development and use
as they progress you get:
-greater gram - activity
-some with less gram + activity (2)
-less B lactamase sensitivity
-cephalosporinase resistant (4)
-less toxic
-better distribution (especially to CNS)
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24
Q

first gen ceph

A

cefazolin
cephalexin
narrow spectrum
chemoprophylaxis

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25
second gen ceph
cefuroxime cefotetan cefaclor intermediate spectrum
26
third gen cep
``` cefotaxime ceftriaxone ceftazidime cefpodoxime broad spectrum ```
27
fourth gen ceph
cefepime | broad spectrum
28
adverse effects of cephs
local irritation from injection renal toxicity--tubular necrosis, interstitial nephritis; may be enhanced by aminoglycosides hypersensitivity - 1% cross reactivity with penicillins, more common in early generation
29
disulfram effect
cefotetan cefoperazone bleeding and platelet disorder (give vitamin K)
30
other B lactams
``` monobactams - aztreonam carbapenems - imipenem meropenem B lactamase inhibitors: -clavulanic acid -sulbactam -tazobactam ```
31
azetreonam
monobactam gram - activity (doesn't work against gram + or anaerobes) B lactamase resistant crosses blood brain barrier no cross reactivity in penicillin-sensitive patients
32
imipenem
``` carbapenems broad spectrum (gram +, Gram -, and anaerobes) B lactamase resistant IV only crosses blood-brain barrier ```
33
discuss the resistance mechanisms to imipenem
pseudomonas develops resistance rapidly, use with aminoglycosides inactivated by renal dipeptidase in host (co administer Cilastatin)
34
meropenem
dipeptidase-resistant carbapenem
35
vancomycin mechanism
``` inhibits transglycosylation (step before transpeptidation) bactericidal for gram + ```
36
vancomycin administration
IV for systemic use | oral for C.diff
37
vancomycin uses
MRSA synergistic w aminoglycosides vancomycin dependent enterococci
38
vancomycin excretion
IV drug cleared through kidney
39
vancomycin adverse effects
enhances oto- and renal toxicity of aminoglycosides red neck syndrome - histamine release misuse/overuse issues
40
fosfomycin
newest ICWS | gram + and gram -
41
fosfomycin mechanism
inhibits cytoplasmic step in cell wall precursor synthesis | active uptake by G6P transporter
42
fosfomycin administration
oral and parenteral oral only in US single dose therapy for UTI
43
fosfomycin metabolism and excretion
excreted by kidney | synergistic w B-lactams, aminoglycosides, or fluororquinolones
44
bacitracin
markedly nephrotoxic topical ONLY OTC
45
B lactamase inhibitors:
- clavulanic acid - sulbactam - tazobactam
46
membrane active drugs
polymixin B | polymixin E
47
polymixin mechanism
basic peptides, act as detergents
48
polymixin uses
gram - EXCEPT proteus and Neisseria limited to topical use due to systemic toxicity (renal) salvage therapy for highly resistant Acinetobacter, Pseudomonas, and Enterobacterieae
49
give an overview of the inhibitors of protein synthesis (IPS) drug class as a whole
target is "different" in pathogen than host due to differing ribosome sizes different sites for different drugs (30S vs 50S) different steps in protein synthesis blocked by different drugs most reversible and bacteriostatic (except aminoglycosides) less selective toxicity than ICWS
50
tetracyclines mechanism
reversible binding to 30S subunit bacteriostatic selectivity based on bacterial uptake
51
tetracyclines pharmacokinetics
urually oral, but absorption variable chelate metal ions not absorbed (do not administer w food) rarely given IV
52
tetracyclines distribution
well distributed, except to CNS and synovial fluid concentrates in teeth, bone, liver, kidney cross the placenta and are excreted in milk
53
tetracyclines excretion
doxycycline mostly fecal | others mostly urine
54
clinical uses of tetracyclines
first broad spectrum antibiotic gram + and gram - mycoplasma, chlamydia, rickettsiae Lyme disease
55
tetracycline adverse effects
GI irritation superinfections impaired liver function (high doses, during pregnancy, pre existing liver disease) photosensitization calcium chelation (discoloration, growth retardation, deformity)
56
resistance to tetracyclines
decreased uptake, efflux pumps are major mediators altered ribosomal proteins or RNA are secondary mechanisms (pseudomonas, proteus) indiscriminate use/overuse has fostered emergence of resistance
57
new tetracyclines
glycylcyclines (tigecycline) retain antibacterial spectrum but overcome resistance not affected by efflux pump black box warning due to increased risk of death
58
other tetracyclines
tetracycline doxycycline minocycline
59
macrolide antibiotics
erythromycin clarithromycin azithromycin bacteriostatic or cidal depending on dose
60
macrolide pharmacokinetics
``` absorbed from GI tract, but acid labile use enteric coating or erythromycin esters also administered IV excellent distribution except to CNS crosses placenta excreted in bile half life 1-5 hours EXCEPT azithromycin ```
61
clinical uses of macrolides
gram + bacteria, same gram - some mycobacteria backup for penicillins in pen--sensitive patients azithro and clarithro are broader spectrum mycoplasma pneumonia, Legionnaires, chlamydia
62
macrolides adverse effects
1. GI distress 2. microsomal enzyme inhibition (drug-drug interactions, oral anticoagulant, digoxin, non sedating antihistamines) 3. hepatotoxicity
63
macrolide resistance
staph resistant, some strepto and pneumococci - altered rRNA - efflux pump - esterase which hydrolyzes erythromycins
64
clarithromycin
less GI effects | longer half life (6 hours)
65
azithromycin
minimal p450 based interactinos tissue levels 10-100 x higher than plasma levels t0.5= 2-4 days
66
newer macrolides in general
clarith and azith both higher availability active against mycobacterium avium-intracellulare in AIDS patients
67
macrolide like: ketolide
telithromycin (semi synthetic macrolide)
68
telithromycin administration
oral well absorbed and distributed metabolized in liver and excreted in bile and urine once daily dosing
69
telithromycin uses
resp tract infections (CAP, bronchitis, sinusitis) | poor substrate for efflux pump
70
telithromycin adverse effects
inhibits CYP3A4 | QT prolongation
71
aminoglycosides mechanism
bactericidal irreversible inactivation of 30S ribosome | multiple effects on translation, misreading of mRNA, interference with initiation, breaking up polysomes
72
aminoglycosides pharmacokinetics
``` poor oral absorption, usually IV or IM good distribution, except eye and CNS no significant host metabolism excreted unchanges very high conc in proximal tubule cells ```
73
aminoglycosides cell killing type
``` concentration dependent (also fluoroquinolones) peak serum concentration related to extent of killing higher peak = increased efficacy ```
74
aminoglycoside drugs
``` gentamycin (older) tobramycin amikacin streptomycin (older) neomycin spectinomycin ```
75
aminoglycoside uses
non resistant gram - infections E.coli, proteus, pseudomonas use older first, save newer for when they're needed
76
when treating pseudomonas w aminoglycosides...
use gentamicin > tobramycin >amikacin
77
spectinomycin use
used against pen resistant gonococci
78
adverse effects of aminoglycosides
``` nephrotoxicity -high concentration in renal cortes -5-25% receiving more than 3 days show renal impairment -usually reversible ototoxicity -high conc in inner ear 5-25% of patients -may be reversible -loss of vestibular and/or auditory function ```
79
dose and time dependency of aminoglycosides
plasma conc and time at high conc are critical factors in adverse effects monitor closely once daily dosing
80
neuromuscular blockade of aminoglycosides
very high dose phenomenon most common during surgery also in myasthenia gravis patients
81
aminoglycosides resistance
emerges rapidly is used alone increased bacterial metabolism alteration in bacterial uptake altered target
82
chloramphenicol mechanism
bacteriostatic | broad spectrum
83
chloramphenicol pharmacokinetics
well absorbed from all routes CNS levels = serum levels 100% excreted in urine glucuronidation in liver is rate limiting step for inactivation/clearance
84
chloramphenicol resistance
plasmid mediated chloramphenicol acyl transferase slow development only slight resistance
85
chloramphenicol adverse effects
GI disturbances followed by fungal superinfections anemia due to bone marrow depression aplastic anemia (irreversible and often fatal) gray baby syndrome (cant clear drug) drug-drug interactions
86
chloramphenicol clinical uses
powerful, but use limited by toxicity and resistance typhoid fever rocky mountain spotted fever
87
clindamycin mechanism
lincosamide antibiotic bacteriostatic well absorbed and distributed
88
clindamycin uses
bacteroides fragilis, other anaerobes MRSA endocarditis prophylaxis
89
clindamycin adverse effects
GI upset C. difficile superinfections hepatotoxicity
90
what are the streptogramins
quinupristin | dalfopristin
91
streptogramins mechanism
peptide macrolactones potent inhibitor of CYP 3A4 block sites affected by macrolides and clindamycin
92
streptogramins uses
bacteriostatic against enterococcus faecium bactericidal against others approved for use against vanco- and multi drug resistant enterococcus faecium, and MRSA
93
streptogramins administration
IV 80% excreted in bile, 20% excreted in urine no cross resistance with any other IPS
94
oxazolidinones (linezolid) mechanism
prevents formation of 70S ribosome | no cross resistance with other IPS
95
linezolid administration
IV or oral | good distribution to tissues
96
linezolid uses
bactericidal against streptococci bacteriostatic against staphylococci and enterococci primary indication - vancomycin resistant E. faecium
97
linezolid adverse effects
bone marrow suppression | thrombocytopenia (reversible and mild)
98
what are the two classes of anti-folates
inhibitors of folate synthesis -p-Aminobenzoic acid analogs (PABA) inhibitors of folate use -dihydrofolate reductase inhibitors
99
sulfonamides
sulfamethoxazole sulfasalazine (salicylazosulfapyridine) silver sulfadiazine co-trimoxazole
100
sulfonamides mechanism
PABA analogs enter into a normal metabolic pathway, but then block the pathway competitive inhibitor of dihydrofolate synthesis bacteriostatic
101
sulfonamide pharmacokinetics
``` oral, some topical (burns), rarely IV well absorbed from GI, well distributed including to CNS variable metabolism acetylation yields inactive metabolite excreted in urine 10-20x blood conc in urine ```
102
clinical uses of sulfonamides
topical for burns (silver) UTI ulcerative colitis (sulfasalazine) rarely used as single agents (combine with trimethoprim)
103
sulfonamide adverse effects
``` allergic reactions: fever, rash -up to 5% incidence -may cross react with other sulfonamides stevens-johnson syndrome -fever, malaise, rare but can be fatal crystalluria/hematuria hematopoietic effects hemolytic anemias ```
104
sulfonamide resistance
overproduction of PABA loss of permeability new form of dihydropteroate synthetase (discriminated between PABA and sulfonamide)
105
which drug exhibits dihydrofolate reductase inhibition activity?
trimethoprim- blocks bacterial enzyme
106
trimethoprim administration
readily absorbed from GI wide distribution, including CNS excreted in urine
107
trimethoprim uses
can be used alone for UTI, but usually combined with a sulfonamide trimethoprim-sulfamethoxazole (co-trimoxazole) pneumocystis pneumonia combo is bactericidal
108
trimethoprim adverse effects
``` 10000x more effective against bacterial DHFR than mammalian, but still may see "anti-folate" effects megaloblastic anemia leukopenia granulocytopenia treat with folinic acid ```
109
AIDS patients receiving co-trimoxazole
``` much higher incidence of adverse effects fever rashes leukopenia diarrhea ```
110
DNA gyrase inhibitors
``` quinolones -nalidixic acid fluoroquinolones -ciprofloxacin -levofloxacin ```
111
DNA gyrase inhibitor mechanism
nalidixic acid: -inhibits bacterial topoisomerase II; transcription, and DNA replication -inhibits bacterial topoisomerase IV; DNA replication fluoroquinolones: -fluorinated analogues of nalidixic acid
112
fluoroquinolones pharmacokinetics
well absorbed and distributed oral (parenteral forms available too) 20% is metabolized in liver excreted in urine
113
fluoroquinolones use
excellent for gram - moderate for gram + gram - in GI and UTIs promise for resp, skin, and soft tissue infections -- especially for multi drug resistant organisms
114
fluoroquinolones adverse effects
``` some GI Less: -headaches -dizziness -insomnia -abnormal liver function connective tissue disorder? ```
115
drugs used as urinary tract antiseptics
use systemic agents which are efficiently cleared in urine | -pens, aminoglycosides, sulfas, fluoroquinolones
116
issues w urinary tract antiseptics
resistance and reinfection common | may need to suppress bacteria for a long time
117
alternative drug for urinary tract
nitrofurantoin
118
nitrofurantoin mechanism
unknown, maybe oxidative stress | bacteriostatic or cidal depending on organism
119
nitrofurantoin pharmacokinetics
rapidly absorbed, metabolized and excreted in urine oral NOT systemic even as IV
120
clinical use of nitrofurantoin
UTI, gram + or gram - | most effective if urine pH < 5.5
121
nitrofurantoin adverse effects
anorexia GI distrubances occasional hemolytic anemia, leukopenia, hepatotoxicity
122
nitrofurantoin resistance
all pseudomonas | some proteus
123
when is anti-mycobacterial chemotherapy used
tuberculosis and leprosy chronic infections with long dormant period separating intermittent active (symptomatic) periods intracellular pathogens
124
duration of anti-tuberculosis therapies
``` uncomplicated - 6-9 mo chemoprophylaxis - 1 year TB meningitis - 2 years resistance develops rapidly to single drugs combo is the general rule ```
125
1st line anti-mycobacterials
``` isoniazid ethambutol rifampin streptomycin pyrazinamide dapson ```
126
2nd line anti-mycobacterials
cycloserine ethionamide capreomycin para-aminosalicylic acid (PAS)
127
isoniazid mechanism
blocks synthesis of mycolic acids for cell wall | bactericidal in growing cells only
128
isoniazid pharmacokinetics
well absorbed and distributed oral CNS 20-100% of serum; intracellular = extracellular acetylated in liver fast acetylators require higher doses -50% of US blacks and whites, most Asians, native americans excreted in urine
129
isoniazid clinical uses
prophylaxis - used alone | combo therapy for TB - w ethambutol, rifampin, or pyrazinamide
130
isoniazid adverse effects
dose and duration dependent hepatotoxicity peripheral and central neuropathy (treat with pyridoxine)
131
isoniazid resistance
rapid development 10% of US isolates higher in Caribbean and asia (20%) deletion of katG gener in mycobacterium
132
rifampin mechanism
inhibits bacterial RNA synthesis | bactericidal
133
rifampin pharmacokinetics
well absorbed and distributed | excreted in bile
134
rifampin adverse effects
inducer of microsomal enzymes (alters t0.5 of anticoagulants, oral contraceptives, other drugs) hepatotoxic flu like syndrome orange body fluids
135
clinical use of rifampin
combination chemo for active disease | single agent prophylaxis for INH intolerant patients or INH resistant bug
136
ethambutol mechanism
inhibits synthesis of mycobacterial cell wall glycan
137
ethambutol pharmacokinetics
well absorbed and distributed CNS levels variable, but usually therapeutic most excreted in urine
138
ethambutol adverse effects
dose dependent optic neutitis decreased acuity loss of red green differentiation
139
pyrazinamide pharmacokinetics
oral absorbed and distributed bacteriostatic
140
pyrazinamide mechanism
activated by mycobacterium blocks membrane functions rapid resistance if used alone
141
pyrazinamide adverse effects
causes hyperuricemia (gouty arthritis) in up to 40% 1-5% incidence of hepatotoxicity contraindicated in pregnancy
142
what is characteristic of 2nd line anti-TB drugs?
toxicity outweighs therapeutic effects except for highly resistant strains -PAS, cycloserine, ethionamide currently a resurgence in TB, highly resistant strains are common
143
what drug is used to treat leprosy?
dapsone
144
dapsone pharmacokinetics
well absorbed and distributed concentrates in skin, muscle, liver, and kidney acetylated and excreted in feces and urine
145
dapsone adverse effects
hemolysis | methemoglobinemia
146
dapsone uses
used in combo with rifampin and clofazimine for M. leprae | P. jroveci pneumonia
147
bactericidal drugs
``` aminoglycosides bacitracinB lactams isoniazid metronidazole polymixins pyrazinamide quinolones quinpristin-dalfopristin rifampin vancomycin ```
148
bacteriostatic drugs
``` chloramphenicol clindamycin ethambutol linezolid macrolides nitrofurantoin sulfonamides tetrcyclines trimethoprim ```
149
why shouldn't you combine static and cidal drugs?
cidal inhibit cells that are growing | if you stop growth with a static agent, there is nothing for the cidal agent to kill
150
ototoxic drugs
aminoglycosides | vancomycin
151
hematopoietic toxic drugs
chloramphenicol | sulfonamides
152
hepatotoxic drugs
tetracyclines isoniazid erythromycin clindamycin
153
renal toxic drugs
cephalosporins vancomycin aminoglycosides sulfonamides

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