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micro chapter 4 final > ya rab > Flashcards

ya rab Flashcards

1
Q

what does cephalosporins inhibit?

A

cell wall synthesis

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2
Q

what are cephalosporins made of?

A

beta lectam ring infused with 6-membered dihydrothiazine ring (cephen nucleus)

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3
Q

what does the sidechine confers in cephalosporins

A
  1. an improved spectrum
  2. pharmacokinetic advantages
  3. additional side effects
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4
Q

how many gens of cephalosporins are there

A

5

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5
Q

what does the activity against G+ depends on in cephalosporins

A

affinity for penicillin binding proteins

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6
Q

what does the activity against G- Depends on in cephalosporins?

A

penetration through the outer membrane

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7
Q

are cephalosporins sicidal or static? is it concentraion dependent?

A 
bactericidal 
concentraion independed (4-5 times the MIC)
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8
Q

why are cephalosporins better than penicillin?

A
  1. less side effects
  2. resistant to penicillinase
  3. effective against G-
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9
Q

what are Gen1 cephalosporins?

A

cephazolin
cephalexin
cephalosporin
all have (PHA)

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10
Q

what are gen 2 cephalosporins?

A 
cefotaxitin 
cefotetan
cefprozil
cefaclor 
(cant help you here but memorize all the gens and anything else is this)
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11
Q

what are the gen 3 cephalosporins

A

( IME ONE DINIR please)
cefotaxIME
ceftriaxONE
cefDINIR

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12
Q

what are the gen 4 cephalosporins

A 
PI
cefePIme (resistants to beta lectamase, broad range)
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13
Q

what are gen 5 cephalosporins?

A

ROL

ceftaROLine (good against MRSA and VRSA)

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14
Q

what are B lacatmase resistant cephalosporins?

A

cefotaxIME (gen3)
cefamandole gen2
cefuroxime gen 2
cefoxitin gen 2

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15
Q

what are the anti pseudomonal cephalosporins

A 
( The DIME DINE ZONE)
ceftazidime 
cefsulodine
cefoperazone 
all gen 3
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16
Q

how does the bacteria resist cephalosporins

A
  1. beta lectamase
  2. altered affinity
  3. decreased the penetraion of antibiotics to the target site (only gram -)
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17
Q

what is the spectrum for gen 1 cephalosporins?

A
  1. G- aerobs (PEcK)
  2. G+ aerobic cocci ( strepto pyogenes, methicillin resistant stap, strepto pneumoniae)
  3. anarobic in the oral cavity

PEck= proteus, E.coli and klebsiella

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18
Q

what is the spectrum for gen 2 cephalosporins

A

Gram + aerobic cocci (same as gen 1)
anaerobes most that are in the mouth and colon ( those are gram -)

stronger than gen 1 at gram -

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19
Q

what is the spectrum for gen 3 cephalosporins

A
  1. improved against enterobacteriacea (hospital infection)
  2. G+ aerobic cocci ( S.aureus)
  3. G- aerobes HiMN-PEcK
  4. anarobic in the oral cavity

HiMN= hemophilus influenzae, moraxella, neisseria

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20
Q

what is the fourth gen spectrum in cephalosprins

A

1.G+ aerobic cocci: strepto pneumoniae, MSSA
2.G- aerobes:pseudomans
not active against anaerobes

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21
Q

what is the spectrum for gen 5 cephalosporins

A

MRSA
VRSA
pseudomonal

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22
Q

regarding Carbapenems what are the following?
the spectrum
side effects
examples

A

extreme broad spectrum
seizures
example Imipenem

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23
Q

whats the problem with Imipenem

A

its very resistante to lectamase but its hydrolyzed by kideny dehydropeptidase enzyme
we give Imipenem with cilastatin ( dehydropeptidase inhibitor)

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24
Q

regarding monobactams what are the following
example
is it related to penicillin

A

Aztreonam: low toxicity and high activity against G-

yes its related to synthertic penicillin

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25
Q

what are the beta lactam antibiotics?

A

penicillins
cephalosporins
carbapenems
monobactams

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26
Q

what are the non beta lectams that inhibit cell wall synthesis

A
  1. glycopeptides—-vancomycin

2. polypeptides—-bacitarcin and polymyxin

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27
Q 
regarding vancomycin what are the following 
spectrum 
bactericidal or static 
how does it work 
biggest weakness
A

works against G+ and MRSA

bactericidal

inhibits cell wall peptidoglycan synthesis

biggest weakness is VRE

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28
Q 
regarding Bacitracin what are the following 
spectrum 
how does it work 
uses 
side effect
A

G-

inhibits cell wall synthesis at early stages by interfering with Bactoprenol

topical use only

high toxicity

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29
Q

what is polymyxin spectrum with an example

A

Colistin works on many types of G- but not G+

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30
Q

what are the mycolic acid inhibitor drugs

A

Isoniazid and Ethambutol

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31
Q

regarding isoniazid answer the following

the spectrum and uses

A

used against mycolic acid bacteria

used to treat tuberculosis along with ethanbutol and rifampin

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32
Q

what is rifampin

A

bactericidal against G+ and TB and some G-

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33
Q

regarding Ethambutol answer the following
how does it work
spectrum

A

block the assembly of arabinogalactan by inhibtion of arabinotransferase enzyme

works only against mycobacterium (secondary drug)

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34
Q

the prokaryotic cells have 70s that concisit of 30s (one mole of rRNA) and 50s (two moles of rRNA)

A

true

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35
Q

eukaryotes have 80s that concist of 40s and 60s sub units

A

true

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36
Q

what drugs attack the 30s subunite

A

1.tetracycline
ex chlorotetracycline , oxytetracycline, minocycline and doxycycline

  1. glycyclines
    ex tigecycline
  2. aminoglycosides
    ex streptomycin, neomycin, gentamicin, kanamycin , tobramycin
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37
Q 
regarding aminoglycoside answer the following 
is it bactericidal
whats the MOA 
how can we enhance it 
whats the side effects 
give some examples
A

yes it is ya habibi

  1. binds to the ribosome
  2. blocks the formation of initiation complex

by increasing the active uptake of the bacteria

ototoxicity and neurotoxicity

streptomycin 
kanamycin 
amikacin
gentamicin
neomycin 
torbramycin
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38
Q

regarding streptomycin talk about the following
what makes it special
its effects
its disadvantages

A

its the oldest and most well known treatment for TB

two effects
1. inhibit protein synthesis by preventing the assembly of ribosome by blocking the initiation steo (static)

  1. misreading of codon by distortion of the 30s subuint (bactericidal)

biggest disadvantages are ototoxicity and development of resistance

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39
Q 
what are the uses for th following 
neomycin 
gentamicin
tobramycin 
kanamycin
A

neomycin otc topical, skin and eye

gentamicin good against pseudomonas

tobramycin eye infiction

kanamycin active in low concentraion against tb

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40
Q

regarding tetracycline group answer the following
the spectrum
is it bactericidal
examples on natrual and semi-synthetic tetracycylines

A

borad spectrum

no its bacteriostatic

natrual: tetracycline, oxytetracycline, chlortytracycline

semi-synthetic: doxycycline and minocycline

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41
Q

whats the MAO of tetracyclines

A

binds with the 30s and stops the attachment of tRNA carrying amino acids to the mRNA-ribosome complex

42
Q

do tetracyclines effect 30s and 40s or only 40s?

A

both 30s and 40s

43
Q

tetracyclines dont effect mammalian cells….why?

A

because the depends on the active uptake by bacteria which doesnt happen in mammalian cells

44
Q 
regarding tetracyclines answer the following 
what do we use it for 
the side effects 
not advised for who?
what are the resistances against it
A

we used it for obligated intracellular like rikesttsia and chlamydia
we also used it for UTI and walking pneumonia

side effects are: upset GI, phototoxicity, superinfections (by candida albicans), brown teeth on children, and kideny damage after expiration

not adviced for children and pregnant woman

resistant to tetracycline by

  1. failure of the active uptake
  2. active efflux pump
45
Q

what are glycylcycline give example advantages disadvanages and uses

A

similar in structuare to tetracycline

example is tygecycline

advantage is the inhibtion of the rapid efflux

the disadvantage is should be taken by slow IV

used against MRSA and acinetobacter baumanii

46
Q

name the drugs that inhibits 50s subunit

A
  1. chloramphenicol
  2. macrolids (erthromycin, azithromycin and clarithomycin)
  3. streprogramins (dalfopristin and quinupristin)
  4. lincomycin and clindamycin
  5. oxazolidinons (linezoild)
  6. fusidic acid
47
Q 
what are the folloeing regarding chloranphenicol 
spectrum
is  it bacteriostatic 
biggest disadvantage 
how is it taken
A

board spectrum
bacteriostatic

it has serious toxicity problems and can cause plastic anemia

can be taken orally as a tasteless med
can be taken parentally as chloramphenicol sodium succinate

48
Q

what is the MOA of chloramphenicol

A

enters the bacteria by facilitated diffusion

stops the aminoacyl tRNA from binding to the accptor site stopping the peptidyltransferase from forming peptide bond

49
Q

can chloramphenicol penetrate mammalian cells and used against intracellular pathogens

A

yes

50
Q

can chloramphenicol inhibit mitochondrial protein sysnthis because its simmlar in both 70s and 80s

A

yes

51
Q

from where did macrolide get their name

A

from macarocycylic lactone ring

52
Q

whats the MAO for erythomycin

A

stops the transloaction step in 50s subunit

53
Q

whats the spectrum for erythomycin and its uses

A

same spectrum as penicillin G

used for legionellosis and mycoplasma pneumonia

54
Q

what are azalides (azithromycin and claritheomycin)

A

boarder spectrum macrolides with better penetraion and diarrhea as a side effect

55
Q

give an exmaple on semisynthetic macrolides

A

ketolides such as telithromycin

56
Q

what is the MOA of streptogramins (dalfopristin and quinupristin)

A

dalfopristin blocks early protein synthesis

quinupristin blocks a step later

57
Q

what is synercid

A

a combination of quinupristin and dalfopristin

used for MRSA and VRE

the combination is synergistic and bactericidal

broad range of G+

58
Q

what is the MOA, spectrum , and biggest problem of lincomycin and clindamycin

A

they block the inhibtion of peptidyl transferase

G+ve except enterococcus faecalis

cross resistance my accor with macroloides and streptogramin

59
Q

what is the spectrum and example on oxazolidinons

A

good against VRE, MRSA and bacteria that are not sensitive against synercid

example lineazolid

60
Q

what are the specreum effect and uses of fusidic acid

A

bacterio static
used in creams and eyedrops
effects the elogation factor
works on G+ only

61
Q

what drugs deals damage to the plasma membrane

A

polymyxin

62
Q

whats polymyxin spectrum, effect and side effects

A

works on the LPS of G-

bactericidal

neurotoxicity, nephrotoxicity and RBCs toxicity

63
Q

what drugs act on inhbition of nucleic acid

A

rifampicin (transcription process)
quinolones (dna replicantion)
nitrofurantion (damage of dna)

64
Q

regarding rifampicin anwser the following the spectrum

uses, effect, side effects and MOA

A

gram positive cocci
bactericidal for mycobacterium along with isoniazid
used to treat tb and leprosy
turns body fulids to orange and heptatotoxic

can reach the csf where tb is loctaed and inhibits the transcription process

65
Q

regarding quinolones what are the following

spectrum uses effect examples side effects and MOA

A

broad spectrum

bactericidal

used to treat UTI

the first drug was nalidixic acid
norfloxcin and ciprofloxacin are fluoroquinolones (semi-synthetic)
moaxifloxacin and gatifloxacin are 3rd gen with broad spectrum

side effects are interfere with cartilage development in joints ( dont not give to children and pregnant woman)

it inhibits dna gyrase therefore dna replication

66
Q

regarding nitrofuration give the following

uses an example and MAO

A

used for UTI because its mostly active in acidic ph

nitrofurazone is used for burns,wounds and ear infection

it works by flavoproteins who reduces nitrofuran

67
Q

what does folic acid does in bacteria and protozoa

A

can not take up DHF and THF
DHF synthesis from PABA
DHF is reduced to THD by DHFR
THF is used to synthesis DNA&RNA

68
Q

what dse folic acid does in mammalian cells

A

DHF is supplied by diet
DHF is reduced to THF by DHFR
THF is used to synthesis DNA&RNA

69
Q

does sulfoamides effect our cells and why

A

no because it attacks DHF synthesis which only happens in bacteria

70
Q

does methotrexate effect our cells? and why

A

in theroy it does, but in reality it doesnt due to the low affinity to the drug which makes it effective to treat bacteria and cancer

71
Q

what are sulfonamides and trimethoprim

A

bacteriostatic

used to treat UTI

usually used as a synergitic drug

side effects are crystallurine,anemia, patients with glucose-6-phosphate cant use it

72
Q

what anti-fungal effects the sterol (cell wall)

A

polyene (amphotericin B)

azole ( imidazole, clotrimazole,ketoconazole,triazole)

73
Q

whats the diffince between animal streol and fungal streol

A

in fungal its ergosterol

in animals cholestreol

74
Q

answer the following about amphotericin B (polyenes)
from where is it produced
uses
disadvantages

A

produced by strepromyces soil bacteria

used for systemic infection

toxic to kidenys but can be reduced by lipids (liposomes)

poorly absorbed by GIT

given by IV

75
Q

talk about nystatine

A

a polyene
specific against C.albicans
poorly absorbed by GIT
used orally

76
Q

what was the first azole drug

A

imidazole

77
Q

why do we use clotrimazole and miconazole

A

for athletes foot and vaginal yeast infection

78
Q

how can we use ketoconazole

A

can be taken orally for systemic and topical for local

79
Q

whats a triazole antibiotic

A

a fluconazole can be taken orally or iv

80
Q

give an example for allylamines

A

terbinafine and naftifine

81
Q

give a drug that effects the cell wall in fungis

A

Echinocandins

used in aspergillus and candida infection

82
Q

give an example for a durg that effect the cell division

A

Griseofulvin
slowacting
works against ring worm and albican

83
Q

give example for drugd that effects nucleic acids in fungi

A

flucytosine which has a high toxicity to kidneys and bone marrow and narrow spectrum

the selective toxicty due to the fungal coverting it to 5-fluorouracil

84
Q

what are the uses for tolnaftate,undercylenic acid and pentamidine

A

tolnaftate is used for athlete foot

undecylenic acid is used for athlete foot (fatty acid)

pentamidine is used against pneumicystis pneumonia

85
Q

why is it difficult to target virus without damaging the damaging the host

A

because the virus replicate wirhin the cells

86
Q

what do most anti viral drugs include

A

nucleoside and nucleotide analogs

87
Q

how do antiviral agents work

A
  1. preventing the adsorption of viral particle
  2. preventing intracellular penetration
  3. inhibiton of protein or nucleic acid synthesis
88
Q

give an example on non nucleosides analog anti viral drug

A

amantadine and rimantadine

prevent viral penetration
narrow spectrum
used prophylactically against influenza A

89
Q

give an example for influenza treatment

A

zanamivir and oseltamivir

they inhbit neuraminidase (used to spreate the virus from the cell)

90
Q

what is zidovudine (azidothymidine)

nucleosides analogue

A

anti-rettovirus and used to treat AIDS by inhibinting the reverse transcriptase

91
Q 
what are 
acyclovir
ganciclovir
ribavrin 
(nucleosides analogue)
A

acyclovir (inhibits viral dna polymerase, only active against herpes infected cells, resemble deoxyguanosine)

ganciclovir: 100x more active than acyclovir and more toxic ‘
ribavrin: resemble guanine and accelerate the mutation rate

92
Q

give an example for protease inhibitor anti-viral drug

A

Atazanavir

used to control last stage HIV

93
Q

what is the MOA of interferons

A

• Proteins produced by virus infected host cell in very small amounts

  • Diffuse to uninfected neighboring cells
  • React with plasma or nuclear membrane receptors
  • They induce the uninfected cells to manufacture mRNA for synthesis of antiviral proteins (AVPs)
  • AVPs are enzymes that disrupt various stages of viral multiplication
94
Q

what are the types of interferons

A

• Two types of interferon;
1. Type I; two classes; alfa IFN and beta IFN
❖Alfa INF is the drug of choice for Viral hepatitis infection
2. Type II; gamma INF, called immune INF produced by Tlymphocyte
❖Causes neutrophils and macrophages to phagocytize
bacteria

Interferons prevent spread of viruses to new cells

95
Q 
what are the following 
quinie
chloroquine
quinacrine 
diiodohydroxyquin
tinidazol
ornidazole
A
  1. Quinine
    • Used to treat malaria
    • Artemisinin and artemisinin-based combination therapies (ACTs),
    have become the principal treatment of malaria.
  2. Chloroquine
    • Synthetic derivative of quinine
    • Inhibit DNA synthesis
  3. Quinacrine
    • Drug of choice for treating protozoan disease giardiasis
  4. Diiodohydroxyquin (Iodoquinol)
    • Effective against amoeba
    • Dosage must be carefully adjusted to avoid optic nerve damage
  5. Metronidazole and Tinidazol
    • Active against parasitic protozoa and obligatory anaerobic bacteria
    • MOA; damages DNA and interfere with anaerobic metabolism
    • Used to treat;
    1.Giardiasis
    2.Amoebic dysentery
    3.Vaginitis caused by Trichomonas vaginalis
  6. Ornidazole
    • Active against Entamoebia histolytica, Giardia lamblia.
    • Also, active against anaerobic bacteria e.g. Bacteroides, clostridium,
    Fusobacterium and anaerobic cocci.
    • Bound to plasma proteins and used twice daily for 1-5 days (t½ up to 13
    days in blood).
    • Long-acting tablets
96
Q 
how to treat the following 
• Tapeworms (Taenia saginata)
• Flukes (Fasciola) 
• Roundworms (Ascaris)
• Hookworms (Ancylostoma)
• Pinworms (Enterobius
A

. Prevent ATP generation (Tapeworms)

  1. Alters membrane permeability (Flatworms)
  2. Neuromuscular block (Intestinal roundworms)
  3. Inhibits nutrient absorption (Intestinal roundworms)
  4. Paralyzes worm (Intestinal roundworms)
97
Q

give examples for antihelminthic drugs

A
  1. Niclosamide
    ❖ MOA; Prevents ATP generation
    ➢ Treatment of Tapeworms
2. Praziquantel
• MOA; Alters membrane permeability
• It cause the helminthes to undergo muscular spasm and make it susceptible to 
attack by the immune system
• Broad spectrum
➢ Treatment of Flatworms
  1. Mebendazole & albendazole
    • MOA; Inhibits nutrient absorption
    • Drug of choice to treat Intestinal roundworms (nematodes)
4. Ivermectin
• MOA; Paralyzes worm
• Drug of choice to treat 
oIntestinal roundworms
oHead lice
98
Q

how to prevent the resistance of antibiotics

A

. Patients should always finish the full regimen of their antibiotic
prescriptions to discourage the survival and proliferation of the
antibiotic-resistant microbes.

  1. Patients should never use leftover antibiotics to treat new illnesses
    or use antibiotics that were prescribed to someone else.
  2. Prescribing the most specific antibiotic possible, instead of broadspectrum antimicrobials,
  3. Avoid injection of antibiotics in air by nurses. Bacteria of nostril of
    hospital workers become resistant to antibiotics and can be
    transmitted to patients as nosocomial. Inserting the needle into sterile cotton can prevent aerosols from forming
99
Q

what is the future of chemotherapeutic agents

A
  1. Target their virulence factors rather than the microbe producing them
  2. The use of antimicrobial peptides produces by many birds, amphibians, plants, and mammals.
  3. knowledge of the basic genetic structure of microbes that may help us to identify new targets for antimicrobials.
  4. The development of fully synthetic molecules (such as the quinolones
    and the oxazolidinones) will be of increasing importance.
  5. The use of phage therapy : bacteriophage, viruses that attack bacteria, were capable of killing specific pathogenic bacteria.
  6. Serendipity, or accidental discovery, is always a consideration. For example, a. quinolones, nalidixic acid, was discovered as an intermediate in the synthesis of an antimalarial drug,
    b. chloroquine, and that the oxazolidinones were originally developed to treat
    plant diseases.
  7. Finally, there is a special need for new drugs act as antiviral ,antibacterial,
    antifungal, and antiparasites (protozoans and helminths)
100
Q

i love you

A

i love you too

micro chapter 4 final (1 decks)

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