ya rab Flashcards
(100 cards)
1
Q
what does cephalosporins inhibit?
A
cell wall synthesis
2
Q
what are cephalosporins made of?
A
beta lectam ring infused with 6-membered dihydrothiazine ring (cephen nucleus)
3
Q
what does the sidechine confers in cephalosporins
A
- an improved spectrum
- pharmacokinetic advantages
- additional side effects
4
Q
how many gens of cephalosporins are there
A
5
5
Q
what does the activity against G+ depends on in cephalosporins
A
affinity for penicillin binding proteins
6
Q
what does the activity against G- Depends on in cephalosporins?
A
penetration through the outer membrane
7
Q
are cephalosporins sicidal or static? is it concentraion dependent?
A
bactericidal concentraion independed (4-5 times the MIC)
8
Q
why are cephalosporins better than penicillin?
A
- less side effects
- resistant to penicillinase
- effective against G-
9
Q
what are Gen1 cephalosporins?
A
cephazolin
cephalexin
cephalosporin
all have (PHA)
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)
11
Q
what are the gen 3 cephalosporins
A
( IME ONE DINIR please)
cefotaxIME
ceftriaxONE
cefDINIR
12
Q
what are the gen 4 cephalosporins
A
PI cefePIme (resistants to beta lectamase, broad range)
13
Q
what are gen 5 cephalosporins?
A
ROL
ceftaROLine (good against MRSA and VRSA)
14
Q
what are B lacatmase resistant cephalosporins?
A
cefotaxIME (gen3)
cefamandole gen2
cefuroxime gen 2
cefoxitin gen 2
15
Q
what are the anti pseudomonal cephalosporins
A
( The DIME DINE ZONE) ceftazidime cefsulodine cefoperazone all gen 3
16
Q
how does the bacteria resist cephalosporins
A
- beta lectamase
- altered affinity
- decreased the penetraion of antibiotics to the target site (only gram -)
17
Q
what is the spectrum for gen 1 cephalosporins?
A
- G- aerobs (PEcK)
- G+ aerobic cocci ( strepto pyogenes, methicillin resistant stap, strepto pneumoniae)
- anarobic in the oral cavity
PEck= proteus, E.coli and klebsiella
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 -
19
Q
what is the spectrum for gen 3 cephalosporins
A
- improved against enterobacteriacea (hospital infection)
- G+ aerobic cocci ( S.aureus)
- G- aerobes HiMN-PEcK
- anarobic in the oral cavity
HiMN= hemophilus influenzae, moraxella, neisseria
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
21
Q
what is the spectrum for gen 5 cephalosporins
A
MRSA
VRSA
pseudomonal
22
Q
regarding Carbapenems what are the following?
the spectrum
side effects
examples
A
extreme broad spectrum
seizures
example Imipenem
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)
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
25
what are the beta lactam antibiotics?
penicillins
cephalosporins
carbapenems
monobactams
26
what are the non beta lectams that inhibit cell wall synthesis
1. glycopeptides----vancomycin
| 2. polypeptides----bacitarcin and polymyxin
27
```
regarding vancomycin what are the following
spectrum
bactericidal or static
how does it work
biggest weakness
```
works against G+ and MRSA
bactericidal
inhibits cell wall peptidoglycan synthesis
biggest weakness is VRE
28
```
regarding Bacitracin what are the following
spectrum
how does it work
uses
side effect
```
G-
inhibits cell wall synthesis at early stages by interfering with Bactoprenol
topical use only
high toxicity
29
what is polymyxin spectrum with an example
Colistin works on many types of G- but not G+
30
what are the mycolic acid inhibitor drugs
Isoniazid and Ethambutol
31
regarding isoniazid answer the following
| the spectrum and uses
used against mycolic acid bacteria
used to treat tuberculosis along with ethanbutol and rifampin
32
what is rifampin
bactericidal against G+ and TB and some G-
33
regarding Ethambutol answer the following
how does it work
spectrum
block the assembly of arabinogalactan by inhibtion of arabinotransferase enzyme
works only against mycobacterium (secondary drug)
34
the prokaryotic cells have 70s that concisit of 30s (one mole of rRNA) and 50s (two moles of rRNA)
true
35
eukaryotes have 80s that concist of 40s and 60s sub units
true
36
what drugs attack the 30s subunite
1.tetracycline
ex chlorotetracycline , oxytetracycline, minocycline and doxycycline
2. glycyclines
ex tigecycline
3. aminoglycosides
ex streptomycin, neomycin, gentamicin, kanamycin , tobramycin
37
```
regarding aminoglycoside answer the following
is it bactericidal
whats the MOA
how can we enhance it
whats the side effects
give some examples
```
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
```
38
regarding streptomycin talk about the following
what makes it special
its effects
its disadvantages
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)
2. misreading of codon by distortion of the 30s subuint (bactericidal)
biggest disadvantages are ototoxicity and development of resistance
39
```
what are the uses for th following
neomycin
gentamicin
tobramycin
kanamycin
```
neomycin otc topical, skin and eye
gentamicin good against pseudomonas
tobramycin eye infiction
kanamycin active in low concentraion against tb
40
regarding tetracycline group answer the following
the spectrum
is it bactericidal
examples on natrual and semi-synthetic tetracycylines
borad spectrum
no its bacteriostatic
natrual: tetracycline, oxytetracycline, chlortytracycline
semi-synthetic: doxycycline and minocycline
41
whats the MAO of tetracyclines
binds with the 30s and stops the attachment of tRNA carrying amino acids to the mRNA-ribosome complex
42
do tetracyclines effect 30s and 40s or only 40s?
both 30s and 40s
43
tetracyclines dont effect mammalian cells....why?
because the depends on the active uptake by bacteria which doesnt happen in mammalian cells
44
```
regarding tetracyclines answer the following
what do we use it for
the side effects
not advised for who?
what are the resistances against it
```
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
what are glycylcycline give example advantages disadvanages and uses
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
name the drugs that inhibits 50s subunit
1. chloramphenicol
2. macrolids (erthromycin, azithromycin and clarithomycin)
3. streprogramins (dalfopristin and quinupristin)
4. lincomycin and clindamycin
5. oxazolidinons (linezoild)
6. fusidic acid
47
```
what are the folloeing regarding chloranphenicol
spectrum
is it bacteriostatic
biggest disadvantage
how is it taken
```
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
what is the MOA of chloramphenicol
enters the bacteria by facilitated diffusion
stops the aminoacyl tRNA from binding to the accptor site stopping the peptidyltransferase from forming peptide bond
49
can chloramphenicol penetrate mammalian cells and used against intracellular pathogens
yes
50
can chloramphenicol inhibit mitochondrial protein sysnthis because its simmlar in both 70s and 80s
yes
51
from where did macrolide get their name
from macarocycylic lactone ring
52
whats the MAO for erythomycin
stops the transloaction step in 50s subunit
53
whats the spectrum for erythomycin and its uses
same spectrum as penicillin G
used for legionellosis and mycoplasma pneumonia
54
what are azalides (azithromycin and claritheomycin)
boarder spectrum macrolides with better penetraion and diarrhea as a side effect
55
give an exmaple on semisynthetic macrolides
ketolides such as telithromycin
56
what is the MOA of streptogramins (dalfopristin and quinupristin)
dalfopristin blocks early protein synthesis
| quinupristin blocks a step later
57
what is synercid
a combination of quinupristin and dalfopristin
used for MRSA and VRE
the combination is synergistic and bactericidal
broad range of G+
58
what is the MOA, spectrum , and biggest problem of lincomycin and clindamycin
they block the inhibtion of peptidyl transferase
G+ve except enterococcus faecalis
cross resistance my accor with macroloides and streptogramin
59
what is the spectrum and example on oxazolidinons
good against VRE, MRSA and bacteria that are not sensitive against synercid
example lineazolid
60
what are the specreum effect and uses of fusidic acid
bacterio static
used in creams and eyedrops
effects the elogation factor
works on G+ only
61
what drugs deals damage to the plasma membrane
polymyxin
62
whats polymyxin spectrum, effect and side effects
works on the LPS of G-
bactericidal
neurotoxicity, nephrotoxicity and RBCs toxicity
63
what drugs act on inhbition of nucleic acid
rifampicin (transcription process)
quinolones (dna replicantion)
nitrofurantion (damage of dna)
64
regarding rifampicin anwser the following the spectrum
| uses, effect, side effects and MOA
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
regarding quinolones what are the following
| spectrum uses effect examples side effects and MOA
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
regarding nitrofuration give the following
| uses an example and MAO
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
what does folic acid does in bacteria and protozoa
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
what dse folic acid does in mammalian cells
DHF is supplied by diet
DHF is reduced to THF by DHFR
THF is used to synthesis DNA&RNA
69
does sulfoamides effect our cells and why
no because it attacks DHF synthesis which only happens in bacteria
70
does methotrexate effect our cells? and why
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
what are sulfonamides and trimethoprim
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
what anti-fungal effects the sterol (cell wall)
polyene (amphotericin B)
| azole ( imidazole, clotrimazole,ketoconazole,triazole)
73
whats the diffince between animal streol and fungal streol
in fungal its ergosterol
| in animals cholestreol
74
answer the following about amphotericin B (polyenes)
from where is it produced
uses
disadvantages
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
talk about nystatine
a polyene
specific against C.albicans
poorly absorbed by GIT
used orally
76
what was the first azole drug
imidazole
77
why do we use clotrimazole and miconazole
for athletes foot and vaginal yeast infection
78
how can we use ketoconazole
can be taken orally for systemic and topical for local
79
whats a triazole antibiotic
a fluconazole can be taken orally or iv
80
give an example for allylamines
terbinafine and naftifine
81
give a drug that effects the cell wall in fungis
Echinocandins
| used in aspergillus and candida infection
82
give an example for a durg that effect the cell division
Griseofulvin
slowacting
works against ring worm and albican
83
give example for drugd that effects nucleic acids in fungi
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
what are the uses for tolnaftate,undercylenic acid and pentamidine
tolnaftate is used for athlete foot
undecylenic acid is used for athlete foot (fatty acid)
pentamidine is used against pneumicystis pneumonia
85
why is it difficult to target virus without damaging the damaging the host
because the virus replicate wirhin the cells
86
what do most anti viral drugs include
nucleoside and nucleotide analogs
87
how do antiviral agents work
1. preventing the adsorption of viral particle
2. preventing intracellular penetration
3. inhibiton of protein or nucleic acid synthesis
88
give an example on non nucleosides analog anti viral drug
amantadine and rimantadine
prevent viral penetration
narrow spectrum
used prophylactically against influenza A
89
give an example for influenza treatment
zanamivir and oseltamivir
they inhbit neuraminidase (used to spreate the virus from the cell)
90
what is zidovudine (azidothymidine)
| nucleosides analogue
anti-rettovirus and used to treat AIDS by inhibinting the reverse transcriptase
91
```
what are
acyclovir
ganciclovir
ribavrin
(nucleosides analogue)
```
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
give an example for protease inhibitor anti-viral drug
Atazanavir
used to control last stage HIV
93
what is the MOA of interferons
• 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
what are the types of interferons
• 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
```
what are the following
quinie
chloroquine
quinacrine
diiodohydroxyquin
tinidazol
ornidazole
```
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
```
how to treat the following
• Tapeworms (Taenia saginata)
• Flukes (Fasciola)
• Roundworms (Ascaris)
• Hookworms (Ancylostoma)
• Pinworms (Enterobius
```
. Prevent ATP generation (Tapeworms)
2. Alters membrane permeability (Flatworms)
3. Neuromuscular block (Intestinal roundworms)
4. Inhibits nutrient absorption (Intestinal roundworms)
5. Paralyzes worm (Intestinal roundworms)
97
give examples for antihelminthic drugs
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
```
3. 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
how to prevent the resistance of antibiotics
. Patients should always finish the full regimen of their antibiotic
prescriptions to discourage the survival and proliferation of the
antibiotic-resistant microbes.
2. Patients should never use leftover antibiotics to treat new illnesses
or use antibiotics that were prescribed to someone else.
3. Prescribing the most specific antibiotic possible, instead of broadspectrum antimicrobials,
4. 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
what is the future of chemotherapeutic agents
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
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