all the antibiotics (kill me pls)

what are the macrolides

what are the macrolides

erythromycin, clarithromycin, azithromycin

route of erythro

po and iv

route of clarithro

po

route of azithro

iv and po

macrolides moa

bind to 50s ribosomal subunit, inhibiting protein synthesis via blocking of transpeptidation/translocation reactions

are macrolides bacteiostatic or bacteriocidal

static

most common macrolide resistance mechanisms

reduced permeability or active efflux. and modificstion of the ribosomal binding site by a macrolide-inducible or constitutive methylase

are macrolides time or conc. dependant and why

time and idk why because they have PAEs but apparently azithro is conc

are macrolides absorbed well orally

no

which macrolide must be taken on an empty stomach

erythromycin base,PCE, or sterate

macrolide ADRs

stomach discomfort (erythromycin worst), taste disturbances (clarithromycin), QT prolongation, drug int

which macrolide has worst coverage

erythro

coverage of macrolides

very poor gram +

better gram - for resp pathogens (h flu except erythro, all cover m cattarrhalis)

chlamidophilia

azithro covers salmonella shigella

what is azithro DOC for

chlamydia trachomatis

what are the tetracyclines

doxy,mino,tetra

tetracyclines route

all po

tetracyclines moa

bind to 30s ribosomal subunit, inhibiting protein synthesis

most common mechanism of bacterial resistance for tetracyclines

decreased intracellular accumulation due to efflux by active transport protein pump

are tetracyclines bacteriostatic or cidal

static

are tetracyclines time or conc dependant

time (but they have PAEs)

which tetracyclines are absorbed well orally

all except tetra

which tetracyclines should be taken with food

mino,doxy - avoid milk

which tetra should be taken on empty stomach

tetra

tetracycline ADRs

GI upset, esophageal ulceration with doxy, photosensitivity, discolored baby teeth, vestibular side effects, bind to divalent cations (AVOID W MILK), least likely to cause c diff

tetracycline coverage

MSSA, MRSA (except tetra), h flu/mcat, peptostrep, chlamydophilia and m pneumoniae

what is doxy DOC in

chlamidophilia and m pneumoniae (walking pneumonia), chlamydia

what are all tetracyclines DOC in

M pneumoniae

what are the quinolones

ciprofloxacin, norfloxacin, levofloxacin, moxifloxacin

cipro route

IV and PO

norfloxacin route

po

levo route

IV and PO

moxi route

IV and PO

what coverage do flouroquinolones widely lack

gram +

flouroquinolones moa

block bacterial DNA synthesis by inhibiting bacterial topoisomerase II (DNA gyrase) and topoisomerase IV

which quinolone is least likely to get resistance

moxifloxacin

what leads to moxifloxacin resistance

overuse and inapropriate use of cipro and levo

are quinolones bacteriocidal or static

cidal

are quinolones conc or time dependant

conc

which quinolone does not require renal adjustment

moxi

most common ADR with quinolones

GI upset

quinolones other adrs

qt prolongation, photosensitivity, binds to divalent cations, affects sugars, cns toxicity, arthropathy, tendinopathy, risk of aortic rupture

quinolone coverage

strep and staph (NOT CIPRO), all easy to kill gram - except n meningitidis, all SPACE except actinobacter and moxi has no pseudomonas, chlamidophilia and m pneumonia

what is cipro DOC in

shigella, pseudomonas

what is levo DOC in

h flu, shigella, pseudomonas, chlamidophilia, chlamydia trachomatis

what is moxi DOC in

h flu, chlamophilia,

which quinolones include pseudomonas

cipro,levo

which quinolone(s) (possibly) treat bfrag

moxi

what are the aminoglycosides

gentamycin,tobramycin,amikacin

route of aminoglycosides

IV

aminoglycosides MOA

binds to 30s subunit ribosomal proteins and results in defective cell membrane

are aminoglycosides bactericidal or static

cidal

is aminoglycoside killing time or conc. dependant

concentration

how long is aminoglycosides post antibiotic effect

6 hrs

aminoglycoside ADR

nephrotoxicity (see less now due to od dosing), ototoxicity, neuromuscular blockade

what type of coverage do aminoglycosides have

gram -

when do aminoglycosides have gram + coverage

synergistically (ex: gentamycin + vancomycin)

aminoglycosides bacteria coverage

easy to kill g-:e coli, shigella, salmonella, kleibsella, proteus

most hard to kill g- (except acinetobacter)

vancomycin route

IV and PO

vancomycin moa

inhibits cell wall synthesis by binding to the D-Ala-D-Ala terminus of nascent peptidoglycan pentapeptide. this inhibits transglcosylase, preventing further elongation of peptidoglycan and cross linking. peptidoglycan is weakened and the cell becomes susceptible to lysis and cell membrane is damaged

is vancomycin killing time or conc dependant

time

what route of vancomycin is used to treat c diff

po

is vancomycin bactericidal or static

cidal

vancomycin resistance mechanisms

due to synthesis of unusually thickened walls (more peptidoglycan layers), the vancomycin binds to the extra layers and becomes sequestered within the cell wall and is unable to reach site of action. (VRE, VISA)

due to modification of the D-Ala-D-Ala binding site of the peptidoglycan building block in which the terminal D-Ala is replaced by D-lactate, resulting in loss of a critical hydrogen bond that facilitates high affinity binding of vancomycin to its target (VRSA)

what type of coverage does vancomycin have

gram + only basically

what is vancomycin DOC for

viridians strep, MSSA, C diff (PO), MRSA, enterococcus

when should vancomycin be reserved for

when other antibiotics cannot be used due to ADR/allergies, or when bacteria is resistant to other antibiotics

vancomycin ADRs

infusion reactions, ototoxicity (uncommon but can occur with consistently high peaks), nephrotoxicity (uncommon)

clindamycin route

PO and IV

clindamycin moa

binds to 50s ribosomal subunit, inhibiting protein synthesis

is clindamycin bactericidal or static

static

clindamycin resistance mechanisms

mutation of the ribosomal receptor site, modification of the receptor by a constitutively expressed methylase, enzymatic inactivation of clindamycin

clindamycin coverage

gram + only (strep, mssa, l mono, peptostrep)

clindamycin ADR

diarrhea- most likely to cause C diff

trimethoprim and sulfamethoxazole route

IV and PO

TMP-SMX moa

sulfa- inhibits bacterial synthesis of dihydrofolic acid by compeititon with para-aminobenzoic acid

tmp- blocks production of tetrahydrofolic acid from dihydrofolic acid by reversibly inhibiting the required enzyme, dihydrofolate reductase, bacterial dihydrofolic acid reductase

is TMP-SMX bactericidal or static

cidal together (static on own)

TMP-SMX general coverage type (gram +,-,etc)

variety of gram +, gram - and other miscellaneous

TMP-SMX ADR

NVD, skin rashes (SJS and TEN), photosensitivity, rash, pruritism bone marrow toxicity, increased serum creatinine, increased K, decreased Na and possible crystalluria, possible teratogenicity and increased risk for kernicterus (avoid in third trimester)

nitrofurantoin MOA

drug gets reduced by bacterial flavoproteins to reactive intermediates, which inactivate or alter bacterial ribosomal proteins and other macromolecules, which causes inhibition of vital biochemical processes of aerobic energy metabolism and the synthesis of DNA, RNA, cell wall, protein

where are therapeutic concentrations of nitrofurantoin achieved

urine only

is nitrofurantoin bactericidal or static

cidal

nitrofurantoin coverage type

some gram + and -

what are nitrofurantoin exclusively used for

UTI

ADR of nitrofurantoin

loss of appetite, nausea, vomiting, darkens urine, GI upset, nausea, headache, SJS/TEN (rare), hepatic reactions (rare), neuropathy/pulmonary fibrosis/hepatic fibrosis (long term use), increased risk of hemolysis in those with G6PD deficiency and in the third trimester/delivery with newborn

fosfomycin MOA

inactivates enolpyruvyl transferase, ultimately inhibits bacterial cell wall synthesis. also decreases adherence of bacteria to epithelial cells of the urinary tract

fosfomycin general coverage type

some gram + and some gram -

fosfomycin ADRs

GI upset, diarrhea, headache, hypokalemia

bacteria covered by TMP-SMX

nitrofurantoin bacteria coverage

e coli and klebsiella, s saphrocytes

metronidazole moa

passive diffusion into cytoplasm of anaerobic bacteria where transport proteins such as ferredoxin transfer electrons to the nitro group of metronidazole forming a nitroso free radical, creating a concentration gradient for intracellular transport of metronidazole where the free radical of metronidazole interacts with intracellular DNA resulting in inhibition of DNA synthesis and degradation and ultimately bacterial death

what types of organisms is metronidazole used for

anaerobic, parasitic

metronidazole ADRs

disulfiram like reactions when taken with alcohol (nausea, vomiting, ab cramps, headache), GI upsetm metallic taste, headache, vaginitis, peripheral/optic neuropathy (long term use), neurotoxicity (rare)

moa of beta lactams

bind to penicillin binding proteins (PBP) which cause the peptidoglycan barrier to not form properly, causing cell lysis

most common mechanisms of resistance to beta lactams

enzymatic destruction by beta lactamases and altered PBP binding sites

are beta lactams bacteriocidal or static

cidal

what type of killing do beta lactams have (____ dependant)

time

most common ADR with beta lactams

hypersensitivity reactions

other adrs of beta lactams

hematologic ADRs at high dose/long durations, neurological events at high doses, C diff

what type of rash with penicillin is NOT indicative of a true IgE mediated allergy

delayed rashes after first few doses or days and no itchiness or hives

if someone has non urticaria rash with penicillin can you give beta lactams

when risk of true allergy is low, can use cephalosporin with a dissimilar side chain