12. Mechanism of action-
Potent cidal, Multiplying organisms are suseptible
They weaken bacterial cell wall & interfere with bacterial
cell wall Protein synthesis .
Organisms possess PPBs ( penicillin binding protiens ).They
are diff. for diff. oganisms. This explains their differing
sensitivity to various B-lactum antibiotics.
Rapid cell wall synthesis occurs when the organisms are
rapidly multiplying. This is the phase targeted by Pns.
Positive- cell wall –Peptidoglycan
Negative-cell wall- Peptido. alternates with
lipoprotien
Peptidoglycan – is lysed by Pns. Forming cell wall deficient
leading to bacterial death.This explains,their efficacy in
positive organisms only. (Peptidoglycan is absent in higher
13. Spectrum- Narrow spectrum-Mostly covers Gram positve Cocci than Bacilli.
Natural Pns-Srepto, staph (except penicillinase producing),pneumo,gono,
meningo, B.anthracis, C.dyphtheriae Cl. Tetany, Cl. Welchii, Listeria,
spirochetes, actinomyces, E.coli & Proteus (few strains)
100 % resistance- B. fragilis, Mycobacteria, chlymydiae, Protozoa,
Ricketsiae, Fungi, Viruses
Amino Pns- Above + H.infue, Salmo, Shige, Proteus, Pseudo, Klebsi,
Aerobacter enterococci,
Extended sp.pns- carbena, ticar, piper- Pseudomonas, Proeus,
Azlocillin- 10 times more potent than carbena. Against psedo.
Mezlocillin- highly effective & specific in Klebsiella.
Mecillinam- 100 % resistance in pseudo.No action against staph. &
strepto. Effective in E.coli, salmo, shige, klebsi,
Pivmecillin- MDR Typhoid
15. PnG is still highly effective inPnG is still highly effective in
S.T.D.s - syphilis , gonorrhoea (not all strains )S.T.D.s - syphilis , gonorrhoea (not all strains )
Leptospirosis - ( Cepha, Tetracyclines )Leptospirosis - ( Cepha, Tetracyclines )
Diphtheria – Antitoxin therapy + PnG.Diphtheria – Antitoxin therapy + PnG.
Tetanus & Gas gangreneTetanus & Gas gangrene
Drug of choice in – Anthrax , Actinomycosis, Trench mouth,Drug of choice in – Anthrax , Actinomycosis, Trench mouth,
Rat bite fever & infections caused by Listeria monocytogens ,Rat bite fever & infections caused by Listeria monocytogens ,
Pasteurella multocida.Pasteurella multocida.
Meningococcal infections.Meningococcal infections.
16. Beta-lactamase inhibitorsBeta-lactamase inhibitors
Clavulanic acidClavulanic acid --Streptomyces clavuligerStreptomyces clavuliger
Has beta lactum ring, no antibacterial activity of its ownHas beta lactum ring, no antibacterial activity of its own
Progressive inhibitor of Penicillinase but not MethicillinaseProgressive inhibitor of Penicillinase but not Methicillinase
Main problem – Partial inhibitor of enzyme ( can induceMain problem – Partial inhibitor of enzyme ( can induce
Beta lactamase production in few organisms ). It inhibits classBeta lactamase production in few organisms ). It inhibits class
II to V betalactamase, but not cephalosporinase.II to V betalactamase, but not cephalosporinase.
SulbactumSulbactum – Complete blocker of enzyme. Three times more– Complete blocker of enzyme. Three times more
potent than Clavu. Acid. It is also devoid of antibacterialpotent than Clavu. Acid. It is also devoid of antibacterial
activity.activity.
TozabactumTozabactum- Similar to sulbactum. Combines well with- Similar to sulbactum. Combines well with
pipercillin.pipercillin.
( Rifampicin + amoxy./ cotra./ doxy. )( Rifampicin + amoxy./ cotra./ doxy. )
17. CephalosporinsCephalosporins
1945- Prof.G.Brotzu- sea water culture- Cephalosporium1945- Prof.G.Brotzu- sea water culture- Cephalosporium
acremonium- from this fungus Cephalosporin C is obtained-acremonium- from this fungus Cephalosporin C is obtained-
possess 7-amino cephalosporanic acid nucleus.possess 7-amino cephalosporanic acid nucleus.
Mechanism- all are potent cidals. Mechanism is similar toMechanism- all are potent cidals. Mechanism is similar to
Pns. They inhibit bacterial cell wall synthesis. HoweverPns. They inhibit bacterial cell wall synthesis. However
protiens inhibited are different. Possess better cell wallprotiens inhibited are different. Possess better cell wall
penetration capacity. Thus their spectrum is wider than Pns.penetration capacity. Thus their spectrum is wider than Pns.
Specrum- staph, strepto, pneumo, gono, E.coli, C.diph,Specrum- staph, strepto, pneumo, gono, E.coli, C.diph,
B.fragilis, Proteus, Indol + Proteus, K.pneumonae, S. tyhpi &B.fragilis, Proteus, Indol + Proteus, K.pneumonae, S. tyhpi &
paratyphi, Shigella, Pseudomonasparatyphi, Shigella, Pseudomonas
Principles- 1- useless against streptococci fecalis.Principles- 1- useless against streptococci fecalis.
2- None is choice in anaerobes.2- None is choice in anaerobes.
3- Do not use cephalosporins when equally effective3- Do not use cephalosporins when equally effective
alternative is available.alternative is available.
4- Meningitis- use only- cephotaxime, ceftizoxime,4- Meningitis- use only- cephotaxime, ceftizoxime,
ceftazidime, cephtriaxoneceftazidime, cephtriaxone
19. Principles in practise-
1st
gen.- good in Gm + , weak in Gm –
2nd
gen.- somewhat increased activity than 1st
gen.
equipotent in Gm+ & Gm – infection
3rd
gen.- good in Gm – (better than 2nd
), weak in Gm + (weaker than 1st
)
4th
generation- relatively new drugs (1990s)
Cefepime- similar to 3rd
gen. Highly resistant to B-lactamase
enzymes. Pseudo. Aeruginosa & staph. Aures are also inhibited.
Cefpirome- serious & resistant hospital acquired infections,
septicaemias, resistant respiratory infections. Highly resistant to B-
lactamase enzymes. More potent against Gm + organisms than 3rd
gen.
Covers many Gm – organisms also.
20. • Cephalothin- peni. Producing Staph.Cephalothin- peni. Producing Staph.
• Typhoid- ceftrioxone, Cefotaxime, CefoperazoneTyphoid- ceftrioxone, Cefotaxime, Cefoperazone
•Mixed aero.& anaero. Infections- Cefuroxime or any 3Mixed aero.& anaero. Infections- Cefuroxime or any 3rdrd
gen. drug ( butgen. drug ( but
none is drug of choice )none is drug of choice )
•Resistant Pseudomonas – Ceftazidime & Cefsulodin. Rest are not thatResistant Pseudomonas – Ceftazidime & Cefsulodin. Rest are not that
useful.useful.
•Septicemias- a. 2Septicemias- a. 2ndnd
gen. + metro.gen. + metro.
b. 1b. 1stst
gen. + amino. + metro.gen. + amino. + metro.
•Hospital acqa. Infections- cefotaxime, ceftizoxime, 4Hospital acqa. Infections- cefotaxime, ceftizoxime, 4thth
gen.( cefepime,gen.( cefepime,
cefpirome )cefpirome )
21. MonobactumMonobactum
Aztreonam-Aztreonam- Highly effective against Gm – entericHighly effective against Gm – enteric
bacilli & H. influ. Moderately effective in pseudo.bacilli & H. influ. Moderately effective in pseudo.
Indications –Indications –
1. In patients allergic to Pns. & Cephalosporins.1. In patients allergic to Pns. & Cephalosporins.
2. In hospital acquired infections – Originating from2. In hospital acquired infections – Originating from
urinary, biliary, gastrointestinal & female genitalurinary, biliary, gastrointestinal & female genital
tractstracts..
22. CarbapenemsCarbapenems
ImipenemImipenem- potent & broad spectrum antibiotic. Inhibits most- potent & broad spectrum antibiotic. Inhibits most
B-lactamases. Covers few methicillin resistant organismsB-lactamases. Covers few methicillin resistant organisms
-Pseudo. Listeria. B.fragilis. Cl.defecile. Enterobacteriaceae.-Pseudo. Listeria. B.fragilis. Cl.defecile. Enterobacteriaceae.
( it is rapidly hydrolised by an enzyme dehydropeptidase I.( it is rapidly hydrolised by an enzyme dehydropeptidase I.
Thus it is combined with Cilastin, a reversible inhibitor ofThus it is combined with Cilastin, a reversible inhibitor of
enzyme )enzyme )
Meropenem-Meropenem- not hydrolised.It is reserve drug in seriousnot hydrolised.It is reserve drug in serious
nosocomal infections. Cephalosporin resistant bacteria are alsonosocomal infections. Cephalosporin resistant bacteria are also
covered.( in practice sometimes it is combined withcovered.( in practice sometimes it is combined with
aminoglycosides )aminoglycosides )
Faropenem-Faropenem- Effective orally. More useful inEffective orally. More useful in
ENT,genitourinary & respiratory infections.covers MoraxellaENT,genitourinary & respiratory infections.covers Moraxella
catarrhis.catarrhis.
23. RifamycinsRifamycins
Rifamycim B-Rifamycim B- Group of antibiotics obtained fromGroup of antibiotics obtained from
Strepto. Mediterrani.Strepto. Mediterrani.
Effective in Gm + & Gm – organisms, including Pns.resistantEffective in Gm + & Gm – organisms, including Pns.resistant
bacteria. Higher conc. Useful in resistant E.coli.bacteria. Higher conc. Useful in resistant E.coli.
Australia- Cholecystitis (higher conc. In bile )Australia- Cholecystitis (higher conc. In bile )
Derivatives of Rifamycin B are – Rifampicin, Rifabutane &Derivatives of Rifamycin B are – Rifampicin, Rifabutane &
Rifapentane.Rifapentane.
24. MacrolidesMacrolides
Contain large lactone ring in structure.Contain large lactone ring in structure.
Erythromycin, Roxithromycin.Erythromycin, Roxithromycin.
Clarithromycin, Azithromycin, SpiramycinClarithromycin, Azithromycin, Spiramycin
Mechanism-Mechanism-
Inhibits bacterial protein synthesis by blockingInhibits bacterial protein synthesis by blocking
bacterial ribosome- 50 S subunit. Interferesbacterial ribosome- 50 S subunit. Interferes
with translocation.with translocation.
Synthesis of larger protein is suppressed.Synthesis of larger protein is suppressed.
Action is enhanced in alkaline PH.Action is enhanced in alkaline PH.
Static / cidalStatic / cidal
26. • Drug of choice in-
1. Pneumonia due to mycoplasma pneumonae- 3
weeks
2. Legionellae pneumonia- 3weeks
3. Perteusis- 2 weeks
4. Chancroid – 1 week
•
27. Alternative / 2nd choice
Campylobacter, Chlamydia, Penicillin resistant
staph.
useful in Gm – rods.
C.dyphth.- carrier stat
In Pns. Sensitive patients. (S.A.B.E.- erythro. 250 mg.
bid.)
28. Roxithromycin- long acting, acid stable, spectrum similar to Erythro.
More potent against Br. Cattarrhis, Gard. Vaginalis, Legionella.
Less potent against B.pertussis.
Clarythromycin- Erythro. + Mycobact. Avium complex(MAC), few
atypical mocobacteria , Myco. Leprae , H.pylori
Nowdays preferred in MAC in AIDS patients.
Azithromycin- Azalide group antibiotic.
More effective in MAC, Chlamy., H.ducr. Campulo., N.gonno.,
penicillinase producing staph. Calymmatobacterium granulomatis.
Spiramycin-(Rovamycin)- Toxoplasma – transplacental transmission.
30. Characteristics-Characteristics-
1. amino sugars in glycosidic linkage.1. amino sugars in glycosidic linkage.
2. None is absorbed orally. Extra cellular distribution. Poor CSF2. None is absorbed orally. Extra cellular distribution. Poor CSF
conc.conc.
3. No metabolism. Excreted by glomerular filtration.3. No metabolism. Excreted by glomerular filtration.
4. Mostly against Gm – organism.4. Mostly against Gm – organism.
5. Cross resistance is known in group.5. Cross resistance is known in group.
6. Their activity is maximum in alkaline Ph.6. Their activity is maximum in alkaline Ph.
7. Similar spectra of toxicity.- oto, nephro & neuro-muscular7. Similar spectra of toxicity.- oto, nephro & neuro-muscular
blockade.blockade.
8. Show synergism with Pns. & Cephalosporins. ( but not in the8. Show synergism with Pns. & Cephalosporins. ( but not in the
same syringe.)same syringe.)
31. Streptomycin-Streptomycin- bacteriocidal, mostly in Gm –bacteriocidal, mostly in Gm –
organismsorganisms
Mechanism- Capable of breaking / penetrating duelMechanism- Capable of breaking / penetrating duel
cell wall of Gm – organ. Combines with bacterialcell wall of Gm – organ. Combines with bacterial
ribosome, 30 S, a sub unit. (others in addition combineribosome, 30 S, a sub unit. (others in addition combine
with 50 S ribosome). This halts initiation of proteinwith 50 S ribosome). This halts initiation of protein
synthesis. They also interfere with mRNA. Makingsynthesis. They also interfere with mRNA. Making
misreading of genetic code. Capable of blockingmisreading of genetic code. Capable of blocking
bacterial enzymes.bacterial enzymes.
Spectrum- E.coli, Shigella, Brucella, Y.pestis,Spectrum- E.coli, Shigella, Brucella, Y.pestis,
Francinella tularensis, Listeria, Nocardia, V. chole.Francinella tularensis, Listeria, Nocardia, V. chole.
Klebsiella, H.ducr, H. infu., Myco.tb.Klebsiella, H.ducr, H. infu., Myco.tb.
32. Role in practice- Drug of choice in Plague (tetra,Role in practice- Drug of choice in Plague (tetra,
chloramph,cotrimo, cipro),chloramph,cotrimo, cipro),
Brucellosis( strepto + tetra, rifampi + cotri /Brucellosis( strepto + tetra, rifampi + cotri /
doxy.,Erythromycin,. ? Spiramycin )doxy.,Erythromycin,. ? Spiramycin )
Tb.- More toxic less effective, higher degree ofTb.- More toxic less effective, higher degree of
resistance , tedious to use (IM route). Expensive. wasresistance , tedious to use (IM route). Expensive. was
added for first 45 to 60 days. Can not go insideadded for first 45 to 60 days. Can not go inside
macrophages. Only multiplying organisms are killed. (macrophages. Only multiplying organisms are killed. (
mycobact.- slow growers )mycobact.- slow growers )
( Nephro, Ototox, Neuromuscular blockade )( Nephro, Ototox, Neuromuscular blockade )
33. Gentamicin-Gentamicin- 20 to 30 times more potent than strepto.20 to 30 times more potent than strepto.
in Pseudomonas.in Pseudomonas.
Effective against –Ps.aeruginosa, Proteus, E.coli,Effective against –Ps.aeruginosa, Proteus, E.coli,
Serratia, Klebsiella, Enterobacter, Many strains ofSerratia, Klebsiella, Enterobacter, Many strains of
strepto.faecalis & staph.aureus.strepto.faecalis & staph.aureus.
Ineffective in- M. Tb., stepto.pyogenes,Ineffective in- M. Tb., stepto.pyogenes,
strepto.pneumoniae.strepto.pneumoniae.
34. Topically effective- eye/ear drops. Solutions.Topically effective- eye/ear drops. Solutions.
Ointments.Ointments.
1.Genta with Pns./Ampi.1.Genta with Pns./Ampi.
2. Genta with carbena./ piper. )2. Genta with carbena./ piper. )
Kanamycin-Kanamycin- Highly ototoxic. Can causeHighly ototoxic. Can cause
respi.arrest or cardiac arrest.respi.arrest or cardiac arrest.
Reserve drug- Fulminating infections, Resistant Tb.,Reserve drug- Fulminating infections, Resistant Tb.,
BrucellosisBrucellosis
35. •Amikacin- Semisynthetic derivative of kanamycin A. Not degraded in
body by enzymes. Used in Genta. Resistant strains. (rest similar to genta)
•Tobramycin- In treatment of Pseudomonas, it is 4 times more potent
than genta. Topical preparations are available.
•Neomycin- from streptomyces fradiae. Highly toxic. Causes 8th
nerve
damage. Not for systemic use. Crude preparation contains A,B & C.
Commercial preparation is mix. Of B & C.
-intestinal asepsis / diarrhoea & dysentery (300 mgs. tid for 5 to 7 days)
-Bladder irrigation
-Hepatic coma- in liver failure intestinal flora grows rapidly causing
ammonia formation. Neomycin kills the flora. (4 to 8 gms./ day )
•
36. Fraymycitin- (Soframycin) It is identical to neomycin
B. Used only topically.
Sisomycin- similar to genta. but more potent.
Netimicin- Klebsiella, Enterobacter,staph, Potent &
less toxic than genta
37. Broad spectrum antibioticsBroad spectrum antibiotics
The true broad spectrum antibiotics areThe true broad spectrum antibiotics are
Tetracyclines (a group) & Chloramphenicol.Tetracyclines (a group) & Chloramphenicol.
Tetracyclines-Tetracyclines- Nucleus of 4 cyclic rings.Nucleus of 4 cyclic rings.
(tetra). Obtained from soil actinomycetes.(tetra). Obtained from soil actinomycetes.
Chlortetracycline is from Stepto.aurofaciens.Chlortetracycline is from Stepto.aurofaciens.
Natural- Oxytetracycline, Tetracycline.( givenNatural- Oxytetracycline, Tetracycline.( given
orally or parenterally )orally or parenterally )
Semisynthetic- demethyl Chlortetracycline,Semisynthetic- demethyl Chlortetracycline,
Doxycycline, Minocycline.Doxycycline, Minocycline.
38. •Mechanism- Bacteriostatic drugs – Main drawback
They are CHELATORS of calcium & magnesium.
Probably this is the main action. They interfere with
bacterial protein synthesis by binding to 30 S
ribosome. Inhibit transfer of m-RNA. (m-RNA-
ribosome complex is not formed. Peptide chain fails to
grow ).
They inhibit bacterial enzymes, but mammalian
enzymes are not inhibited.
39. Spectrum- They cover Gm+ & Gm- bacteria ,
Rickettsiae , Chlamydiae. Few fungi , No action
against viruses.
Resistant organisms – Pseudo. Proteus. Klebsiella ,
Salmo. Bact.fragilis.
Anaerobes are not very sensitive. Mycobact. Were
sensitive.
- Staph, Strepto, Gonno. Meningo. Closridia, Listeria,
Corynebacteria, B.anthracis, Y.pestis, H.ducr.V.chol,
Campylobacter, H.pylori, Brucella, Y.enterocolitica,
P.multocida, Calymmatobacterium granu. Spirochetes.
E.histo. Nocardia. Actinomycosis.
40. • They are 1st
choice in
- Chlamydial urethritis/ cervicitis , L.G.V.,
Granuloma inguinale, Atypical pneumonia due to
Mycoplasma pneumoniae.,Plague, Cholera,
Brucellosis, Relapsing fever, Rickettsial infections
( typhus , Q fever, rocky mountain spotted fever )
42. ChloramphenicolChloramphenicol
From Streptomyces venezuelae – 1947From Streptomyces venezuelae – 1947
Mechanism-Mechanism- Bacteriostatc, H.infl. isBacteriostatc, H.infl. is
exception.exception.
- Interfere with protein synthesis by inhibiting- Interfere with protein synthesis by inhibiting
transfer of peptide chain at mRNA –ribosometransfer of peptide chain at mRNA –ribosome
complex. Gets attached to 50 S ribosome.complex. Gets attached to 50 S ribosome.
- By acting as peptide analogue, it prevents- By acting as peptide analogue, it prevents
formation of petide bonds.formation of petide bonds.
- In high dose- inhibits mammalian- In high dose- inhibits mammalian
mitochondrial protein synthesis. ( Bonemitochondrial protein synthesis. ( Bone
marrow cells )marrow cells )
43. Spectrum-Spectrum- similar to tetracyclines. Tetracyclinesimilar to tetracyclines. Tetracycline
resistant Gmresistant Gm
+ bacteria are usually susceptible to chloramphenocol.+ bacteria are usually susceptible to chloramphenocol.
- H. infu. Psittacosis lympho. Myco.pnemo. V.chol.- H. infu. Psittacosis lympho. Myco.pnemo. V.chol.
E.coli. Brucella. Pasturella. Klebsi. Strepto. pneumo.E.coli. Brucella. Pasturella. Klebsi. Strepto. pneumo.
N. meningitidis. Salmo. S.tyhpi.N. meningitidis. Salmo. S.tyhpi.
44. -In anaerobes it is more potent than tetracyclines.
- Less effective in B.pertu. Klebsi. B.fragilis. Spiro.
Gm + cocci.
- 100% resistance- Myacobact. Entamoeba. Psedo.
Plasmodia. Viruses.
- In chlamydia they are alternatives to tetracyclines.
-Uses- Rarely used.
Enteric fever – resistance, bone marrow depression,
Bacteriostatic ( carrier state is developed ). But in
paratyphoid it is still main stay in treatment.
45. -Anaerobic infections- Respond well ( Metronidazole,
Niridazole, Ticarcillin, 3rd gen.Cephalosporins,
Clindamycin, Carbapenems,)
-Meningitis- H.influ. & Meningococcal meningitis –
Chloramphenicol Is second choice. (nowdays 3rd gen.
cepha. Are 1st line drugs)
-Intraocular infections – high conc. In aqueous fluid.
- Brucellosis & Rickettsial infectios.
46. Miscellaneous antibioticsMiscellaneous antibiotics
Lincosamide antibiotics-Lincosamide antibiotics- LincomycinLincomycin ––
pharmacologically it was choiced drug inpharmacologically it was choiced drug in
osteomyelitis. (higher bone conc.). It covers staph.osteomyelitis. (higher bone conc.). It covers staph.
Penicillinase producing staph. Strepto. Less potentPenicillinase producing staph. Strepto. Less potent
than PnG. Inhibits 50 S ribosome- protein synthesisthan PnG. Inhibits 50 S ribosome- protein synthesis
blocker.blocker. Pseudo-membranous colitis is veryPseudo-membranous colitis is very
common- deathcommon- death
.. Clindamycin- Derivative of Lincomycin .
Bacteriostatic.
used in anaerobic & mixed infections. Bone &
Skin infections respond well.
Pseudo-membranous colitisPseudo-membranous colitis due to clostr. Difficile
is fatal adr. Effect. ( treat it with vancomycin or
Metronidazole )
47. Glycopeptide antibiotic
Vacomycin-Vacomycin- 2nd drug of choice to treat antibiotic2nd drug of choice to treat antibiotic
associated pseudo-membranous enterocolitis due toassociated pseudo-membranous enterocolitis due to
ClostridiumClostridium difficile. (metro.is 1st choice)
Used in oncology departments.
Teicoplanin- More active than vanco. Less toxic.
48. Oxazolidinone antibiotics
• Linezolid- new antibiotic , It stops protein synthesis before it starts.
It binds to 23 S fraction of 50 S ribosome. It interferes with tRNA-70
S initiation complex. Instead of tRNA, the drug Linezolid binds with
either with 30 S or 50 S ribosomal subunits.
• Resistant Gm + cocci, both aerobic & anaerobic are susceptible. Useful
in Methicillinase, Penicillinase resistant bacteria. Few Vancomycin
resistant strains of Staph. Are susceptible.
Strepto.viri.,Strepto.pyogenes, Strepto.pneimo.,Corynebadterium,
Listeria, Clostridia, B.fragalis. Myco.tb.,
Gm – organisms are not inhibited .
• can be given orally or I.V. 84 to 94% primary cure rate.
49. Miscellaneous MicrobicidalsMiscellaneous Microbicidals
• Fucidin-Fucidin- (fucidic acid ) – potent bactericidal on(fucidic acid ) – potent bactericidal on
topical application. (Highly toxic for systemic use.)topical application. (Highly toxic for systemic use.)
Penicillinase staph. Strepto. Are killed . 2% creamPenicillinase staph. Strepto. Are killed . 2% cream
or oint.in wounds,cuts,boils,folliclitis,Psychosisor oint.in wounds,cuts,boils,folliclitis,Psychosis
barbae.etc.barbae.etc.
•Bacitracin-Bacitracin- polypeptide, Used only as cream,polypeptide, Used only as cream,
oint,or dusting powder.oint,or dusting powder.
Staph, Strepto, Gono, Cl. Tetany, Treponema.,Staph, Strepto, Gono, Cl. Tetany, Treponema.,
Enterococci, etcEnterococci, etc
50. Mupirocin-Mupirocin- Developed from PseudomonasDeveloped from Pseudomonas
flurescenes. Potent cidal.flurescenes. Potent cidal.
Very useful in superficial skin infections.Very useful in superficial skin infections.
Covers both Gm+ & Gm-,all strains of Staph. &Covers both Gm+ & Gm-,all strains of Staph. &
Strepto. are covered. 2% oint./cream/powder.Strepto. are covered. 2% oint./cream/powder.
colistin-colistin- (Polymixin E )- from Aerobacillus(Polymixin E )- from Aerobacillus
colistinus.colistinus.
Bactericidal to many Gm – bacteria.Bactericidal to many Gm – bacteria.
H.pertussis, pseudomonas, H.influ., shigella.H.pertussis, pseudomonas, H.influ., shigella.
Highly toxic , rarely used (rather not used ) inHighly toxic , rarely used (rather not used ) in
practice.practice.
51. •Polymixin B - similar to Colistin , but less toxic.Polymixin B - similar to Colistin , but less toxic.
• Spectinomycin-Spectinomycin- (Non aminoglycoside ). From Strepto. Spectabillis(Non aminoglycoside ). From Strepto. Spectabillis
All strains of gono. Are highly susceptible. (2 gms. IM as single dose).All strains of gono. Are highly susceptible. (2 gms. IM as single dose).
Used to treat syphilis. Not popular in India.Used to treat syphilis. Not popular in India.
• FosfomycinFosfomycin- Bactericidal, By inhibiting enzyme, Pyruvyl transerase,- Bactericidal, By inhibiting enzyme, Pyruvyl transerase,
it inhibits bacterial cell wall synthesis.covers both Gm + & Gm –it inhibits bacterial cell wall synthesis.covers both Gm + & Gm –
bacteria. Effective against many urinary pathogens like- E.coli, E.fecalis,bacteria. Effective against many urinary pathogens like- E.coli, E.fecalis,
Klebsi, P.aeruginosa, enterobacter, enterococci, (their all strains areKlebsi, P.aeruginosa, enterobacter, enterococci, (their all strains are
inhibited )inhibited )
In practice Fosfomycin is combined with pipercillin / cefotaxime.In practice Fosfomycin is combined with pipercillin / cefotaxime.
• Tyrothricin-Tyrothricin- Mixture of tyrocidin & gramicidin.Mixture of tyrocidin & gramicidin.
It causes leak in cell wall. Highly toxic for systemic use.( causesIt causes leak in cell wall. Highly toxic for systemic use.( causes
Haemolysis ) Used topically only.Haemolysis ) Used topically only.
Covers most of Gm + & few Gm – bacteria. Resistance development isCovers most of Gm + & few Gm – bacteria. Resistance development is
52. AntihelminthicsAntihelminthics
Mebendazole-Mebendazole- ( Mebex )- broad spectrum( Mebex )- broad spectrum
wormicidalwormicidal
- 100 % - round worms, hook worms, pin- 100 % - round worms, hook worms, pin
worms, whip wormworms, whip worm
- 65 to 75 % - tape worms (H. nana relatively- 65 to 75 % - tape worms (H. nana relatively
insensitive )insensitive )
- Expels trichinella spiralis from intestines.- Expels trichinella spiralis from intestines.
- Probably drug of choice in Oxyuresis.- Probably drug of choice in Oxyuresis.
- Prolonged treatment – Regression in Hydatid- Prolonged treatment – Regression in Hydatid
cyst. ( used post-operatively to preventcyst. ( used post-operatively to prevent
regrowth of cyst )regrowth of cyst )
53. Mechanism- Microtubular protein “ B-tubulin” is siteMechanism- Microtubular protein “ B-tubulin” is site
of action.of action.
It blocks glucose uptake by worm. Glycogen storesIt blocks glucose uptake by worm. Glycogen stores
of worm are depleted leading to Plastic clearance ofof worm are depleted leading to Plastic clearance of
worms. It is lethal to Ascaris ova.worms. It is lethal to Ascaris ova.
- Strictly contraindicated in pregnancy & lactation.- Strictly contraindicated in pregnancy & lactation.
- Rarely required below one year of life.- Rarely required below one year of life.
54. 1. Round worm & Hook worm- 100 mg. bid for 31. Round worm & Hook worm- 100 mg. bid for 3
days. Repeat after one week.days. Repeat after one week.
2. Thread worm- 100 mg. single shot.2. Thread worm- 100 mg. single shot.
3. Tape worms- 200 mg. tid or 300 mg. bid for 33. Tape worms- 200 mg. tid or 300 mg. bid for 3
days. Repeat after one week.days. Repeat after one week.
4. Hydatid cyst- 200 to 400 mg. tid for one month.4. Hydatid cyst- 200 to 400 mg. tid for one month.
( suppresses bone marrow thus not used clinically.)( suppresses bone marrow thus not used clinically.)
Dose- 50 mg. bid for 3 days , below 2 years of age.Dose- 50 mg. bid for 3 days , below 2 years of age.
55. Albendazole -Albendazole - ( Zentel,Bendex,ABZ, Alminth )( Zentel,Bendex,ABZ, Alminth )
below 2 years of age- 200 mg. single shot.below 2 years of age- 200 mg. single shot.
1. Round worm & Hook worm- 400 mg hs. Repeat1. Round worm & Hook worm- 400 mg hs. Repeat
after one week.after one week.
2. Thread worm- 400 mg. single shot.2. Thread worm- 400 mg. single shot.
3. Tape worms- 400 mg. hs. For 3 successive nights.3. Tape worms- 400 mg. hs. For 3 successive nights.
4. Hydatid cyst- 400 mg. bid for one month.(Paed.-4. Hydatid cyst- 400 mg. bid for one month.(Paed.-
10mg/kg. divided in 2 equal doses). Suppression of10mg/kg. divided in 2 equal doses). Suppression of
bone marrow is minimum.bone marrow is minimum.
5. Neurocysticercosis- good alternative to5. Neurocysticercosis- good alternative to
Praziquantel.Praziquantel.
15mg/kg divided in 3 equal doses for 30 days.15mg/kg divided in 3 equal doses for 30 days.
( 400 mg tid )( 400 mg tid )
56. • Round worm ( Ascaris lumbricoid )Round worm ( Ascaris lumbricoid )
Piperazine citrate-Piperazine citrate- round worms & pin wormsround worms & pin worms
Blocks neuromuscular transmission of Ach.inBlocks neuromuscular transmission of Ach.in
parasite causing hyper polarization. – Flaccidparasite causing hyper polarization. – Flaccid
paralysis-paralysis- worm is aliveworm is alive. (Only succinate is reduced. (Only succinate is reduced
causing loss in muscle power.)causing loss in muscle power.)
Safe in pregnancySafe in pregnancy..
Drug of choice in intestinal obstruction due toDrug of choice in intestinal obstruction due to
Round worms. ( Ascarin is not liberated – NoRound worms. ( Ascarin is not liberated – No
endotoxic shock )endotoxic shock )
3.5 gms. on 2 successive nights. (Paed.75 mg / kg.)3.5 gms. on 2 successive nights. (Paed.75 mg / kg.)
57. Pyrantel PamoatePyrantel Pamoate ( Pa-Pa, Nemocid )- round worms &( Pa-Pa, Nemocid )- round worms &
hook wormshook worms
Activates nicotinic cholinergic receptors in worms,Activates nicotinic cholinergic receptors in worms,
resulting into persistent depolarization- spasticresulting into persistent depolarization- spastic
paralysis of worm.paralysis of worm. Worm is killedWorm is killed. (Neuro-. (Neuro-
muscular block.)muscular block.)
600 to 750 mg hs. (Paed.- 10mg/kg.) Hook worm-600 to 750 mg hs. (Paed.- 10mg/kg.) Hook worm-
3 successive nights.3 successive nights.
58. Levamisole- (Dicaris )Levamisole- (Dicaris ) Immunomodulator,Immunomodulator,
Round worm & Hook worm.Round worm & Hook worm.
It causes depolarization block. Worm muscles areIt causes depolarization block. Worm muscles are
contracted. Ach response is blocked. ( Toniccontracted. Ach response is blocked. ( Tonic
paralysis). Worm is killed.paralysis). Worm is killed.
150 mg. single dose. ( Hook worm- repeat after one150 mg. single dose. ( Hook worm- repeat after one
week.)week.)
Mebendazole & Albendazole-Mebendazole & Albendazole-
59. Pin worm / Thread worm ( E. vermicularis)Pin worm / Thread worm ( E. vermicularis)
Mebendazole- 100 mg. single dose.Mebendazole- 100 mg. single dose.
Albendazole- 400 mg. single dose.Albendazole- 400 mg. single dose.
Pyrantel pamoate- 10 mg / kg single dose.Pyrantel pamoate- 10 mg / kg single dose.
Piperazine citrate- alternative drug.Piperazine citrate- alternative drug.
60. Whip worm (Trichuris trichura )Whip worm (Trichuris trichura )
Albendazole or Mebendazole in full dose.Albendazole or Mebendazole in full dose.
Hook worm (Ancylostoma duodenale , NecatorHook worm (Ancylostoma duodenale , Necator
americanus )americanus )
AlbendazoleAlbendazole- 400 mg. for 3 successive nights.- 400 mg. for 3 successive nights.
Mebendazole-Mebendazole- 100 mg bid for 3 days. Repeat after one100 mg bid for 3 days. Repeat after one
week.week.
Pyrantel Pamoate-Pyrantel Pamoate- 600 to 750 mg hs.- 3 successive nights.600 to 750 mg hs.- 3 successive nights.
Bephenium hydrxy naphthoate- ( Alcopar )Bephenium hydrxy naphthoate- ( Alcopar )
5 gm. On empty stomach – saline purge after 2 hours.5 gm. On empty stomach – saline purge after 2 hours.
( Acts by contracting muscles of worm )( Acts by contracting muscles of worm )
61. Guinea worm (Dracunculus medinensis )Guinea worm (Dracunculus medinensis )
NiridazoleNiridazole- highly active drug, ( covers Blood fluke, E. hist,- highly active drug, ( covers Blood fluke, E. hist,
anaerobes )anaerobes )
Inhibits glucose uptake by worms.Inhibits glucose uptake by worms.
25mg /kg /day divided into 4 equal doses for 15 days.25mg /kg /day divided into 4 equal doses for 15 days.
Metronidazole-Metronidazole- similar actionsimilar action
400 mg. tid for 21 days.400 mg. tid for 21 days.
Thiabendazole-Thiabendazole- More toxic than metronidazole.More toxic than metronidazole.
100 mg./ kg /day for 15 days.100 mg./ kg /day for 15 days.
62. Tape wormsTape worms
Niclosamide- (Niclosan 500 mg. tab. )
-Vermicidal drug. Inhibits oxidative
phophorylation & prevents ATP generation.
- T. solium, T. saginata, H. nana., D.lattumT. solium, T. saginata, H. nana., D.lattum
Thread worm.Thread worm.
- T. soli.- Praziquantel is choice.- T. soli.- Praziquantel is choice.
Niclosamide has no action against Ova &Niclosamide has no action against Ova &
chances of auto-infection are always high withchances of auto-infection are always high with
T. soli.T. soli.
- H. nana – relatively insensitive- H. nana – relatively insensitive
63. Dosage- over night fasting.Dosage- over night fasting.
1 gm on empty stomach ( tab. Is chewed )1 gm on empty stomach ( tab. Is chewed )
After 2 hours give 1 gm.After 2 hours give 1 gm.
Wait for next 2 hour.Wait for next 2 hour.
Give saline purge. ( Mag. Sulph.)Give saline purge. ( Mag. Sulph.)
( Purge- digestion of dead segment of T.soli. is hazardous.( Purge- digestion of dead segment of T.soli. is hazardous.
- ova are released causing visceral Cysticercosis.)- ova are released causing visceral Cysticercosis.)
Cure criteria- Absence of eggs & proglottis in stools for 12Cure criteria- Absence of eggs & proglottis in stools for 12
weeks after therapy.weeks after therapy.
64. ChloroquineChloroquine--
2 gm. On empty stomach ( single dose )2 gm. On empty stomach ( single dose )
useful in Fish tape worm.useful in Fish tape worm.
PraziquantelPraziquantel- ( Cysticide, Distocide )- ( Cysticide, Distocide )
It causes leakage of intracellular calcium.It causes leakage of intracellular calcium.
prevents glucose uptake by worms.prevents glucose uptake by worms.
Causes strong contracture in flukes leading to death.Causes strong contracture in flukes leading to death.
Useful in Trematodes, Cestodes & Schistosomes.Useful in Trematodes, Cestodes & Schistosomes.
65. Not recommended below 2 years of age.Not recommended below 2 years of age.
Contraindicated in preg., lact. & ocular cysticercisis.Contraindicated in preg., lact. & ocular cysticercisis.
• Tape worms- ( 100 % cure rate )Tape worms- ( 100 % cure rate )
- T.soli. & T. sagi.- 10 mg./kg single dose.- T.soli. & T. sagi.- 10 mg./kg single dose.
- H.nana & D. latum - 20 mg./kg single dose- H.nana & D. latum - 20 mg./kg single dose..
• Neurocysticercosis- 50 mg / kg / day Divided into 3Neurocysticercosis- 50 mg / kg / day Divided into 3
equal doses for 14 days.equal doses for 14 days.
• S.haematobium- 40 mg./kg single dose.S.haematobium- 40 mg./kg single dose.
Other flukes- 60 mg./kg single dose (s.japonocum &Other flukes- 60 mg./kg single dose (s.japonocum &
s.mansoni ) Fasciola hetatica- partial results.s.mansoni ) Fasciola hetatica- partial results.
66. FilariasisFilariasis
Diethyl carbamazine- (Hetrazan, Banocide )
W.bancrofti, B. malayi, Loa loa, O.volvulusW.bancrofti, B. malayi, Loa loa, O.volvulus
Action- Sensitization of Mf ( microfiliare)Action- Sensitization of Mf ( microfiliare)
membrane. Such sensitized Mf is readilymembrane. Such sensitized Mf is readily
phagocytosed by tissue fixed monocytes, but notphagocytosed by tissue fixed monocytes, but not
by circulating phagocytes.by circulating phagocytes.
Mf is cleared from peripheral blood in 7 days.Mf is cleared from peripheral blood in 7 days.
It increases cell mediated immunity in humans.It increases cell mediated immunity in humans.
Causes hyperpolarization of worms leading toCauses hyperpolarization of worms leading to
dislodgement.dislodgement.
Long term Rx- kills Mf & adult worms.Long term Rx- kills Mf & adult worms.
67. With mass destruction of Mf – release ofWith mass destruction of Mf – release of
allergic protein – fever, lymphadenopathy, skinallergic protein – fever, lymphadenopathy, skin
rash & rarely severe ocular reaction.rash & rarely severe ocular reaction.
Rx- Inj. Hydrocortizone followed by oralRx- Inj. Hydrocortizone followed by oral
Prednesolone.Prednesolone.
( can be prevented by starting DEC in low( can be prevented by starting DEC in low
dose.)dose.)
68. Uses-Uses-
• Filariasis – 2mg/kg tid (100 mg tid ) for 3 weeks.Filariasis – 2mg/kg tid (100 mg tid ) for 3 weeks.
• Tropical eosinophilia-Tropical eosinophilia-
• Larva migrans ( creeping eruption )Larva migrans ( creeping eruption )
Mebendazole is an alternative.Mebendazole is an alternative.
• Onchocercosis due to O. volvulusOnchocercosis due to O. volvulus
no treatment is satisfactory. Condition may causeno treatment is satisfactory. Condition may cause
blindness. Suramin ( highly toxic ) & Ivermectin areblindness. Suramin ( highly toxic ) & Ivermectin are
alternatives.alternatives.
69. IVERMECTIN- (Mectizal, scavista, Vermin )IVERMECTIN- (Mectizal, scavista, Vermin )
from Streptomyces avermitilis.from Streptomyces avermitilis.
It potentiates GABA minergic action in worms. ButIt potentiates GABA minergic action in worms. But
its exact mode of action is unknown.its exact mode of action is unknown.
• Drug of choice in Onchocercosis & strongyloidosisDrug of choice in Onchocercosis & strongyloidosis
in single dose.in single dose.
• Very effective in Filariasis. ( as effective as DEC )Very effective in Filariasis. ( as effective as DEC )
• Highly effective in ascariasis & Cutaneous larvaHighly effective in ascariasis & Cutaneous larva
migrans.migrans.
• Scabies & head lice are killed.Scabies & head lice are killed.
75. (discovered in New-York- Thus Nystatin )(discovered in New-York- Thus Nystatin )
- Candida, Histoplasma, Microsporum, Blastomyc.- Candida, Histoplasma, Microsporum, Blastomyc.
Trichophyton,Trichophyton,
-Mechanism- ill understood, ? Combines with cell-Mechanism- ill understood, ? Combines with cell
membrane & interferes with cellular respiration.membrane & interferes with cellular respiration.
Prevents glucose utilization. Mostly bacteriocidal.Prevents glucose utilization. Mostly bacteriocidal.
- Resistance development is unknown.- Resistance development is unknown.
- Highly toxic for systemic use .- Highly toxic for systemic use .
- In practice used only for candidiasis.- In practice used only for candidiasis.
76. CHLOROPHENSINCHLOROPHENSIN-- old drug, used in Trichomonasold drug, used in Trichomonas
vaginitis, antibacterial & antifungal ( 1% cream )vaginitis, antibacterial & antifungal ( 1% cream )
UNDECYLINIC ACID-UNDECYLINIC ACID-Naturally Present in vagina.Naturally Present in vagina.
effective in acidic PH. ( Doderlin’s Bacilli )effective in acidic PH. ( Doderlin’s Bacilli )
2 to 15 % cream for skin & mucous membranes.2 to 15 % cream for skin & mucous membranes.
TOLNAFTATETOLNAFTATE- ( Tinaderm, Aftate ) – useful in- ( Tinaderm, Aftate ) – useful in
superficial fungal infection & not in candida. It is lesssuperficial fungal infection & not in candida. It is less
effective than Immidazole derivatives. 1 % solution.effective than Immidazole derivatives. 1 % solution.
78. TERBINAFINE- (1 % topical cream)TERBINAFINE- (1 % topical cream)
It is non-competitive blocker of Sqalence epoxidase.It is non-competitive blocker of Sqalence epoxidase.
( enzyme required for early biosynthesis )( enzyme required for early biosynthesis )
Fungicidal, short course of therapy , relapse rate isFungicidal, short course of therapy , relapse rate is
low.low.
Topically active against dermatophytes & candida.Topically active against dermatophytes & candida.
In Onychomycosis it is given orally & appliedIn Onychomycosis it is given orally & applied
simultaneously.simultaneously.
Effectivity in toe nail infection is high. Cure rate isEffectivity in toe nail infection is high. Cure rate is
80 to 90 %.80 to 90 %.
79. BUTENAFINE- ( 1 % cream )BUTENAFINE- ( 1 % cream )
Drivative of Terbinafine.Drivative of Terbinafine.
Mechanism & uses are similar to TerbinafineMechanism & uses are similar to Terbinafine
SODIUM THIOSULFATE- ( 20 % lotion )SODIUM THIOSULFATE- ( 20 % lotion )
weak fungistatic, active against Malassezia furfur.weak fungistatic, active against Malassezia furfur.
Can be used in pityriasis Versi. ( long treatment isCan be used in pityriasis Versi. ( long treatment is
must 3 to 3 weeks.)must 3 to 3 weeks.)
81. Systemic AntifungalsSystemic Antifungals
AMPHOTERICIN B –AMPHOTERICIN B –
Fungistatic or cidal depending on conc.Fungistatic or cidal depending on conc.
High affinity for ergosterol of fungi. Combines withHigh affinity for ergosterol of fungi. Combines with
it, causing micropore in cell wall. Through whichit, causing micropore in cell wall. Through which
amino acids, water soluble substances & ions moveamino acids, water soluble substances & ions move
out.out.
It prevents glucose uptake by fungi.It prevents glucose uptake by fungi.
The cell wall permiability is increased.The cell wall permiability is increased.
82. Spectrum-Spectrum-
candida, histoplasms, cryptococcus, sporotrichum,candida, histoplasms, cryptococcus, sporotrichum,
blastomycosis, coccidiodes, aspergillus, certainblastomycosis, coccidiodes, aspergillus, certain
species of leishmania.species of leishmania.
Higher concentrations are must for Candida.Higher concentrations are must for Candida.
To improve tolerability & to reduce toxicity newTo improve tolerability & to reduce toxicity new
formulations are made available.formulations are made available.
- Amphotercin B lipid complex- Amphotercin B lipid complex
- Amphotercin B colloidal dispersion- Amphotercin B colloidal dispersion
- Liposomal Amphotercin B- Liposomal Amphotercin B
83. EchinocandinsEchinocandins
Anidulafungin , Caspofungin & MicafunginAnidulafungin , Caspofungin & Micafungin
Echinocandins inhibit the synthesis of glucanEchinocandins inhibit the synthesis of glucan
in the cell wall, probably via the enzyme 1,3-βin the cell wall, probably via the enzyme 1,3-β
glucan synthase.glucan synthase.
Caspofungin acetate for injection -TheCaspofungin acetate for injection -The
empirical therapy of presumed fungalempirical therapy of presumed fungal
infections in febrile, neutropenic adult patientsinfections in febrile, neutropenic adult patients
and the treatment of invasive aspergillosis inand the treatment of invasive aspergillosis in
adult patients whose disease is refractory to, oradult patients whose disease is refractory to, or
who are intolerant of, other antifungal agentswho are intolerant of, other antifungal agents
(i.e., conventional or lipid formulations of(i.e., conventional or lipid formulations of
amphotericin B and/or itraconazole). patients.amphotericin B and/or itraconazole). patients.
84. In treatment of candidemia and some specificIn treatment of candidemia and some specific
CandidaCandida infections (intra-abdominal abscesses,infections (intra-abdominal abscesses,
peritonitis, pleural cavity infections and oesophagitis)peritonitis, pleural cavity infections and oesophagitis)
and for the treatment of general invasive candidiasisand for the treatment of general invasive candidiasis
in adult patientsin adult patients
Compared to amphotericin B, caspofungin seems toCompared to amphotericin B, caspofungin seems to
have a relatively low incidence of side-effectshave a relatively low incidence of side-effects..
Anidulafungin & Micafungin have similarAnidulafungin & Micafungin have similar
mechanism & spectrum.mechanism & spectrum.
85. FLUCYTOSINE ( 5-FC ) –FLUCYTOSINE ( 5-FC ) –
Synthetic flurinated pyrimide, a pyrimidineSynthetic flurinated pyrimide, a pyrimidine
antimetabolite. Inside the fungal cell it is convertedantimetabolite. Inside the fungal cell it is converted
into 5-flurouracil inhibiting DNA synthesis.into 5-flurouracil inhibiting DNA synthesis.
- useful in YEAST infections. Cryptococcus,- useful in YEAST infections. Cryptococcus,
Torula, Chromoblastomyces & few strains ofTorula, Chromoblastomyces & few strains of
Candida.Candida.
- Never used alone. Combined with Amphotercin- Never used alone. Combined with Amphotercin
BB
86. GRIESOFULVINGRIESOFULVIN
From Penicillium griesofulvum.From Penicillium griesofulvum.
Most of dermatophytes – Trichophyton,Most of dermatophytes – Trichophyton,
Epidermophyton, Microsporum but no actionEpidermophyton, Microsporum but no action
in Candida & deep mycosis.in Candida & deep mycosis.
Binds to polymerized microtubules &Binds to polymerized microtubules &
disorients them.disorients them.
It reaches keratin forming a barrier betweenIt reaches keratin forming a barrier between
fungus & epidermis. This cuts nutrition offungus & epidermis. This cuts nutrition of
fungi.fungi.
Interferes with purine metabolism of fungus.Interferes with purine metabolism of fungus.
88. Mechanism- The imidazole and triazole drugs areMechanism- The imidazole and triazole drugs are
synthetic antifungal drugs that inhibit the enzymesynthetic antifungal drugs that inhibit the enzyme
cytochrome P450 14α-demethylase. This enzymecytochrome P450 14α-demethylase. This enzyme
converts lanosterol toconverts lanosterol to ergosterolergosterol, and is required in, and is required in
fungal cell membrane synthesis .fungal cell membrane synthesis .
Fortunately they show less affinity for HumanFortunately they show less affinity for Human
cytochrome P 450.cytochrome P 450.
Now a days development of resistance is known.Now a days development of resistance is known.
Particularly it is known with Candida.Particularly it is known with Candida.
89. KETOCONAZOLEKETOCONAZOLE – ( Nizral, Fungicide, Ketovate– ( Nizral, Fungicide, Ketovate
200 mg tab Od or Bid )200 mg tab Od or Bid )
Dermatophytosis & deep Mycosis.Dermatophytosis & deep Mycosis.
NOT USEFUL IN FUNGAL MENINGITIS.NOT USEFUL IN FUNGAL MENINGITIS.
Good concentrations in skin & vaginal fluids.Good concentrations in skin & vaginal fluids.
FLUCONAZOLEFLUCONAZOLE – ( Onecan, Syscan, Forcan,– ( Onecan, Syscan, Forcan,
Zocon 150 mg tab. ) Water soluble triazole.Zocon 150 mg tab. ) Water soluble triazole.
Better & wider activity than ketoconazole.Better & wider activity than ketoconazole.
90. -Systemic & mucosal candidiasis in both normal &-Systemic & mucosal candidiasis in both normal &
immunodeficient patients. 150 mg hs. For 3 nights.immunodeficient patients. 150 mg hs. For 3 nights.
AIDS pts. Once a week for several weeks.AIDS pts. Once a week for several weeks.
Vag. Candidiasis- 150 mg single dose ( for 100 %Vag. Candidiasis- 150 mg single dose ( for 100 %
cure, repeat after 1 week )cure, repeat after 1 week )
Oral thrush- 2 to 4 weeks therapy is must.Oral thrush- 2 to 4 weeks therapy is must.
-Cryptococcl/ Coccidioidal memingitis- 150 mg Bid-Cryptococcl/ Coccidioidal memingitis- 150 mg Bid
for 4 to 12 weeks.for 4 to 12 weeks.
91. - Tinea infections- 150 mg/ week for 4-6 weeks.( In- Tinea infections- 150 mg/ week for 4-6 weeks.( In
Onichomycosis 6 to 12 months )Onichomycosis 6 to 12 months )
- Preferred drug in Fungal meningitis – good CSF- Preferred drug in Fungal meningitis – good CSF
penetration. Here I.V. infusions are used. ( 100 /200penetration. Here I.V. infusions are used. ( 100 /200
mg per bottle )mg per bottle )
- Effective in mucormycosis & aspergillosis.- Effective in mucormycosis & aspergillosis.
NOTE- Fungicidal conc.- skin, brain, CSF., Nails,NOTE- Fungicidal conc.- skin, brain, CSF., Nails,
saliva & vagina.saliva & vagina.
92. ITRACONAZOLE- (ITRACONAZOLE- ( Canditral, Sporanox, ItasporCanditral, Sporanox, Itaspor
100 mg cap. )100 mg cap. )
Broad spectrum but Fungistatic.Broad spectrum but Fungistatic. CSF conc.is poorCSF conc.is poor..
Claimed to be effective in immunocompromisedClaimed to be effective in immunocompromised
pts.pts.
- Better than fluconazole in – Histoplasmiosis,- Better than fluconazole in – Histoplasmiosis,
Blastomycosis, Sporotrichosis. Other spectum isBlastomycosis, Sporotrichosis. Other spectum is
similar to fluconazole.similar to fluconazole.
- No hepatotoxicity, devoid of Steroid inhibition.- No hepatotoxicity, devoid of Steroid inhibition.
Over all toxicity is the lowest.Over all toxicity is the lowest.
93. VORICONAZOLEVORICONAZOLE ––
22ndnd
generation broad spectrum triazole used togeneration broad spectrum triazole used to
treat serious, invasive fungal infections, seen intreat serious, invasive fungal infections, seen in
immunocompromised, and include invasiveimmunocompromised, and include invasive
candidiasis, invasive aspergillosis, and certaincandidiasis, invasive aspergillosis, and certain
emerging fungal infections.emerging fungal infections.
- Febrile neutropenia not responding to antibacterial- Febrile neutropenia not responding to antibacterial
therapy.therapy.
- I.V. followed by oral therapy.- I.V. followed by oral therapy.
94. TERBINAFINETERBINAFINE – ( Lamisil, Sebifin 250 mg tabs. )– ( Lamisil, Sebifin 250 mg tabs. )
Dermatophytes , CandidaDermatophytes , Candida
- Non-competitive blocker of squalence epoxidase- Non-competitive blocker of squalence epoxidase
( an early step enzyme in ergosterol biosynthesis in( an early step enzyme in ergosterol biosynthesis in
fungi )fungi )
- Fungicidal, relapses are rare, short cource of- Fungicidal, relapses are rare, short cource of
treatment.treatment.
- 250 mg Od.- 250 mg Od.
Tinea, T.versocolor, Nail infections.Tinea, T.versocolor, Nail infections.
95. ScabiesScabies
ITCH MITE (sarcoptess scabieivar hominis )ITCH MITE (sarcoptess scabieivar hominis )
Every family member is treated at a time.Every family member is treated at a time.
- Clothes – boil- Clothes – boil
- Scrub the body, take bath then apply to whole- Scrub the body, take bath then apply to whole
body below neck. ( Protect eyes & genitalia )body below neck. ( Protect eyes & genitalia )
- Educate the family about cleanliness.- Educate the family about cleanliness.
Sulphur ointmentSulphur ointment – ( 10 % )– ( 10 % )
Hydrogen sulphide & Parathionic acid – theyHydrogen sulphide & Parathionic acid – they
kill itch mite. Irritant / stains clotheskill itch mite. Irritant / stains clothes
96. Benzyl benzoateBenzyl benzoate – ( 25 %-adults 12.5 % - Kids )– ( 25 %-adults 12.5 % - Kids )
( Dermin , Scabindon )( Dermin , Scabindon )
Drug of choice in kids. Has direct action. AppliedDrug of choice in kids. Has direct action. Applied
for 2 to 3 successive nights for 100 % cure.for 2 to 3 successive nights for 100 % cure.
Non irritant having pungent smell. Itch mayNon irritant having pungent smell. Itch may
persists for 8 days ( Calamine lotion )persists for 8 days ( Calamine lotion )
Gamma benzene hexachlorideGamma benzene hexachloride ( 1% cream or( 1% cream or
lotion- Gammascub, Lindane , Scabex, Ascabiol )lotion- Gammascub, Lindane , Scabex, Ascabiol )
100 % cure with single application.100 % cure with single application.
Avoided in paed. Practice- can cause convulsionsAvoided in paed. Practice- can cause convulsions
or death.or death.
97. Crotamiton – (Crotamiton – (Crotorax, Eurax 10 % Lotion )Crotorax, Eurax 10 % Lotion )
Non irritant , very weak drug, only in infants.Non irritant , very weak drug, only in infants.
PermethrinPermethrin- (Perelice, Lyclear 5 % cream or- (Perelice, Lyclear 5 % cream or
lotion ) Pyrethroid derivative. 100 % cure withlotion ) Pyrethroid derivative. 100 % cure with
2 applications.2 applications.
Monosulphuram SoapMonosulphuram Soap ( Tetmasol ) 25 % .It is( Tetmasol ) 25 % .It is
for prevention than cure.for prevention than cure.
Ivermectin-Ivermectin- ( Scavista, Mectizal )( Scavista, Mectizal )
200 micro grams / kg body wt.- single oral dose200 micro grams / kg body wt.- single oral dose
For 100 % cure.For 100 % cure.
( Antihistaminics & Antibiotics )( Antihistaminics & Antibiotics )
100. Anti-Herpes virus drugsAnti-Herpes virus drugs
IdoxuridineIdoxuridine- Historical drug.- Historical drug.
Acts as thymidine analogue, a pyrimidineActs as thymidine analogue, a pyrimidine
antimetabolite.antimetabolite.
Gets into viral DNA forming Faulty DNA.Gets into viral DNA forming Faulty DNA.
Clinically only in topical treatment of herpesClinically only in topical treatment of herpes
simplex.simplex.
Acyclovir-Acyclovir-
Mechanism-Mechanism-
101. AcyclovirAcyclovir
Acyclovir monophosphateAcyclovir monophosphate
Herpes virus spe.Herpes virus spe.
Thymidine kinaseThymidine kinase
Cellular kinaseCellular kinase
Acyclovir triphosphateAcyclovir triphosphate
Acy. Tri- attaches to DNA preventing its elongation.Acy. Tri- attaches to DNA preventing its elongation.
This inhibits DNA-polymerase inreversibly.This inhibits DNA-polymerase inreversibly.
102. oral Bioavailability is 20 %oral Bioavailability is 20 %
CSF conc. Is 50 % of plasma.CSF conc. Is 50 % of plasma.
Uses-Uses-
1. Genital Herpes simplex1. Genital Herpes simplex
2. Mucocutaneous Herpes simplex2. Mucocutaneous Herpes simplex
3. Herpes simplex encephalitis – Drug of choice3. Herpes simplex encephalitis – Drug of choice
4. Herpes simplex (Type 1 ) keratitis4. Herpes simplex (Type 1 ) keratitis
5. Herpes zoster5. Herpes zoster
6. Chickenpox6. Chickenpox
103. Famciclovir-Famciclovir-
Good oral bioavailability. Long acting. But acyclovirGood oral bioavailability. Long acting. But acyclovir
resistant herpes strains are not inhibited.resistant herpes strains are not inhibited.
Some activity against hepatitis B virus.Some activity against hepatitis B virus.
Valaciclovir-Valaciclovir-
5555 – 70 % oral bioavial.– 70 % oral bioavial.
Pro-drug. After metabolism it is converted intoPro-drug. After metabolism it is converted into
acyclovir.acyclovir.
104. Ganciclovir-Ganciclovir-
Analogue of acyclovir. Covers all Herpeses &Analogue of acyclovir. Covers all Herpeses &
CMV.CMV.
More active in CMV than acyclovir.More active in CMV than acyclovir.
Highly toxic , thus rarely used in practice.Highly toxic , thus rarely used in practice.
Foscarnate-Foscarnate-
simple, straight chain phosphonate which inhibitssimple, straight chain phosphonate which inhibits
viral DNA polymerase & reverse transcriptase.viral DNA polymerase & reverse transcriptase.
- Acyclovir resist. Herpes, Herpes zoster, CMV,- Acyclovir resist. Herpes, Herpes zoster, CMV,
105. Anti-Influenza virus drugsAnti-Influenza virus drugs
Amantidine – ( AAmantidine – ( Amantrel , Neaman )mantrel , Neaman )
Inhibits replication of virus. It interferes withInhibits replication of virus. It interferes with
viral uncoating & Viral assembly. M 2 proteinviral uncoating & Viral assembly. M 2 protein
is targeted.is targeted.
Now a days resistance has developed.Now a days resistance has developed.
( Mutation in M2 protein is cause of Resist. )( Mutation in M2 protein is cause of Resist. )
1. Prophylaxis & treatment of Influenza A21. Prophylaxis & treatment of Influenza A2
( Influenza B is not inhibited ). Can be( Influenza B is not inhibited ). Can be
given along withgiven along with
influenza vaccine.influenza vaccine.
2. Parkinsonism2. Parkinsonism
106. 100 mg Bd. Is the dose. ( kids- 5 mg / kg )100 mg Bd. Is the dose. ( kids- 5 mg / kg )
Rimantadine-Rimantadine-
More potent , long acting & well tolerated.More potent , long acting & well tolerated.
Amantadine resistant virus is resistant toAmantadine resistant virus is resistant to
Rimantidine.Rimantidine.
Dose & uses – similar to AmantadineDose & uses – similar to Amantadine
107. Oseltamivir – ( Tamiflu )Oseltamivir – ( Tamiflu )
Influenza A , B , Bird flu ( H5N1), Swine fluInfluenza A , B , Bird flu ( H5N1), Swine flu
( H1N1)- Amantadine resistant strains are also( H1N1)- Amantadine resistant strains are also
susceptible.susceptible.
It is converted into oseltamivir carboxylate byIt is converted into oseltamivir carboxylate by
liver.- Active metabolite. It acts by inhibiting viralliver.- Active metabolite. It acts by inhibiting viral
Neuraminidase enzyme.Neuraminidase enzyme.
Useful in prophylaxis ( 75 mg Od 10 days) &Useful in prophylaxis ( 75 mg Od 10 days) &
treatment.( 75 mg Bd 5 days ).treatment.( 75 mg Bd 5 days ).
108. ZanamivirZanamivir - ( Relenza )- ( Relenza )
spectrum & action – Similar to Oseltamivir.spectrum & action – Similar to Oseltamivir.
It is POWDER taken by route of INHALATION,It is POWDER taken by route of INHALATION,
as its oral bioavailability is very poor.as its oral bioavailability is very poor.
10 mg is dose. ( contra indicated in Asthmatics –10 mg is dose. ( contra indicated in Asthmatics –
induces bronchospasm by releasing histamine )induces bronchospasm by releasing histamine )
Useful in Oseltamivir resistant strains.Useful in Oseltamivir resistant strains.
Laninamivir- (Laninamivir- ( 1010thth
Aug. 2009 ) – Phase III clinicalAug. 2009 ) – Phase III clinical
trial is going on.trial is going on.
109. Nonselective antiviral drugsNonselective antiviral drugs
RibavirinRibavirin – ( Virazol, Virazide )– ( Virazol, Virazide )
A purine nucleoside analogue having broadA purine nucleoside analogue having broad
spectrum anti viral activity.spectrum anti viral activity.
Influenza A & B, respiratory syncytial virus,Influenza A & B, respiratory syncytial virus,
Many other DNA & double stranded RNAMany other DNA & double stranded RNA
viruses. Probably drug of choice in LASAviruses. Probably drug of choice in LASA
fever.fever.
Intracellular GTP is inhibited. DNA / RNAIntracellular GTP is inhibited. DNA / RNA
synthesis is blocked. ( exact mechanism is notsynthesis is blocked. ( exact mechanism is not
known )known )
110. Given orally / I.V. / nasally.Given orally / I.V. / nasally.
Uses - Influenza A & B, respiratory syncytial virus,Uses - Influenza A & B, respiratory syncytial virus,
Herpes , Measles, Hepatitis B, some rare viralHerpes , Measles, Hepatitis B, some rare viral
infections are susceptible.infections are susceptible.
But in none, it is drug of choiceBut in none, it is drug of choice
Adefovir dipivoxil -Adefovir dipivoxil - ( Adesera , Adfovir )( Adesera , Adfovir )
Active against HBV & some other DNA viruses.Active against HBV & some other DNA viruses.
111. After going into cell Adenofovir monophsphate isAfter going into cell Adenofovir monophsphate is
phosphorylated & coverted into diphosphate. Thisphosphorylated & coverted into diphosphate. This
has affinity for viral DNA polymerase. Thishas affinity for viral DNA polymerase. This
enzyme is inhibited.enzyme is inhibited.
Indicated in chronic hepatitis B or in hepatitisIndicated in chronic hepatitis B or in hepatitis
associated with HIV. ( along with Lamivudine )associated with HIV. ( along with Lamivudine )
InterferonsInterferons --
Are low molecular weight glycoprotein cytokines.Are low molecular weight glycoprotein cytokines.
112. They are produced by host cell in response to viralThey are produced by host cell in response to viral
infections. They have non specific anti-viral actions.infections. They have non specific anti-viral actions.
They interfere with DNA & RNA viruses. TheyThey interfere with DNA & RNA viruses. They
show complex effects on cell proliferation & immuneshow complex effects on cell proliferation & immune
system..system..
Naturally produced as neutralizing antibodies. TheyNaturally produced as neutralizing antibodies. They
exert no action on extra cellular viruses nor preventexert no action on extra cellular viruses nor prevent
cell entry of virus. They increase integrity of hostcell entry of virus. They increase integrity of host
cells. They mostly prevent adsorption. They blockcells. They mostly prevent adsorption. They block
viral transcription.viral transcription.
113. Nothing is known about their fate in body.Nothing is known about their fate in body.
They are species specific but not virus specific.They are species specific but not virus specific.
αα (alpha ) –(alpha ) –From leucocytes infected by viruses.From leucocytes infected by viruses.
β ( beta ) –β ( beta ) – From fibroblastsFrom fibroblasts..
γ ( gamma )-γ ( gamma )- From stimulated T cells ( antigen )From stimulated T cells ( antigen )
114. They are non-toxic, non antigenic , diffusesThey are non-toxic, non antigenic , diffuses
freely & have wide spectrum of activity. Stillfreely & have wide spectrum of activity. Still
in practice they are not promising agents.in practice they are not promising agents.
USES- condyloma acuminata, hepatitis A &USES- condyloma acuminata, hepatitis A &
B , Varicella zoster, Herpes simplex 1 & 2.B , Varicella zoster, Herpes simplex 1 & 2.
prophylactic in CMV. Kaposis sarcoma, hairyprophylactic in CMV. Kaposis sarcoma, hairy
cell leukamia.cell leukamia.
115. GammaglobulinGammaglobulin
It is a blood fraction (Protein ) , synthesized inIt is a blood fraction (Protein ) , synthesized in
body by B lymphocytes. Obtained from serumbody by B lymphocytes. Obtained from serum
called as hyper immune serum. It contains anti-called as hyper immune serum. It contains anti-
bodies.bodies.
Giving gammaglobulin is giving passiveGiving gammaglobulin is giving passive
immunity.immunity.
- Hypo gammaglobulemia, Measles, Rubella,- Hypo gammaglobulemia, Measles, Rubella,
Infective hepatitis, Tetanus , Mumps,Infective hepatitis, Tetanus , Mumps,
Diphtheria, Multiple abscesses, AIDSDiphtheria, Multiple abscesses, AIDS
..
116. Pharmacotherapy of AIDSPharmacotherapy of AIDS
Anti-RetrovirusAnti-Retrovirus
a. Nucleoside reverse transcriptase inhibitorsa. Nucleoside reverse transcriptase inhibitors
Zidovudine, Zalcitabine, StavudineZidovudine, Zalcitabine, Stavudine
b. Non nucleoside reverse transcriptaseb. Non nucleoside reverse transcriptase
inhibitorsinhibitors
Nevirapine, Efavirenze, DelavirdineNevirapine, Efavirenze, Delavirdine
c. Protease inhibitorsc. Protease inhibitors
Ritonavir, Indinavir, Nelfinavir, LopinavirRitonavir, Indinavir, Nelfinavir, Lopinavir
118. Nucleoside containsNucleoside contains a sugar group & base where asa sugar group & base where as
Phosphorylation of nucleoside by Kinases ( additionPhosphorylation of nucleoside by Kinases ( addition
of phosphate in the sugar’s primary alcohol group )of phosphate in the sugar’s primary alcohol group )
produces Nucleotide.produces Nucleotide.
Nucleoside = Sugar + BaseNucleoside = Sugar + Base
Nucleotide = Sugar + Base + PhosphateNucleotide = Sugar + Base + Phosphate
119. combinationscombinations
Preferred –Preferred –
1. 2 NRTI + 1 NNRTI ( no PI )1. 2 NRTI + 1 NNRTI ( no PI )
Zidovudine + lamivudine + efavirenzZidovudine + lamivudine + efavirenz
2. 2 NRTI + 1 PI2. 2 NRTI + 1 PI
Zidovudine + lamivudine + lopinavirZidovudine + lamivudine + lopinavir
AlternativeAlternative
1. 2 NRTI + 1 NNRTI ( no PI )1. 2 NRTI + 1 NNRTI ( no PI )
a. Zidovudine + lamivudine + nevirapinea. Zidovudine + lamivudine + nevirapine
b. stavudine + lamivudine + efavirenzb. stavudine + lamivudine + efavirenz
c. stavudine + lamivudine + nevirapinec. stavudine + lamivudine + nevirapine
2. 2 NRTI + 1 PI2. 2 NRTI + 1 PI
a. Zidovudine + lamivudine + indinavira. Zidovudine + lamivudine + indinavir
b. stavudine + lamivudine + ritonavirb. stavudine + lamivudine + ritonavir
120. 3 NRTI (only when NNRTI & PI are contraindicated – Pt. on3 NRTI (only when NNRTI & PI are contraindicated – Pt. on
Rifampicin therapy ). This is inferior regimen. 3 drugs shouldRifampicin therapy ). This is inferior regimen. 3 drugs should
ideally come from at least 2 different groups.ideally come from at least 2 different groups.
zidovudine + lamivudine + abacavirzidovudine + lamivudine + abacavir
Vertical transmission –Vertical transmission –
only AZT from 3only AZT from 3rdrd
month of pregnancy can minimize the risk.month of pregnancy can minimize the risk.
Many prefer 3 drug regimen.Many prefer 3 drug regimen.
safe drugs in pregnancy are- AZT, lamivudine, nevirapine,safe drugs in pregnancy are- AZT, lamivudine, nevirapine,
nelfinavir saquinqvir etc. ( Lopinavir in last trimester )nelfinavir saquinqvir etc. ( Lopinavir in last trimester )
Post exposure prophylaxisPost exposure prophylaxis
low risk- AZT 300mg + Lamivu. 150 mg BID x 4 weekslow risk- AZT 300mg + Lamivu. 150 mg BID x 4 weeks
high risk- AZT 300mg + Lamivu. 150 mg + Inanavir 800 mghigh risk- AZT 300mg + Lamivu. 150 mg + Inanavir 800 mg
BID x 4 weeksBID x 4 weeks
121. Nucleoside RT InhibitorsNucleoside RT Inhibitors
Zidovudine ( Azidothymidine ) – It is thymidineZidovudine ( Azidothymidine ) – It is thymidine
analogue.analogue.
After phosphorylation in the host cell, zidovudine triphosphateAfter phosphorylation in the host cell, zidovudine triphosphate
inhibits viral reverse transcriptase. ( RNA-dependent DNAinhibits viral reverse transcriptase. ( RNA-dependent DNA
polymerase )polymerase )
Single –stranded viral RNASingle –stranded viral RNA
Virus directed reverse transcriptase
(inhibited by zidovudine triphosphate)
Double –stranded viral DNADouble –stranded viral DNA
122. ( on template of single-stranded RNa genome of HIV( on template of single-stranded RNa genome of HIV
a double stranded DNA copy is produced by virala double stranded DNA copy is produced by viral
reverse transcriptase. ) zidovudine prevents infectionreverse transcriptase. ) zidovudine prevents infection
of new cells by HIV, but has no effect on virusof new cells by HIV, but has no effect on virus
directed DNA that has already integrated into the hostdirected DNA that has already integrated into the host
chromosomes.chromosomes.
Resistance to AZT occurs by point mutations whichResistance to AZT occurs by point mutations which
alter reverse transcriptase enzyme. More than 50 %alter reverse transcriptase enzyme. More than 50 %
patients develop resistance within 1 year if usedpatients develop resistance within 1 year if used
alone.alone.
Par excellent drug- decreases HIV-RNA titer toPar excellent drug- decreases HIV-RNA titer to
undetectable levels & increases CD4 countundetectable levels & increases CD4 count
progressively.progressively.
123. Stavudine –Stavudine – another thymidine analogueanother thymidine analogue..
AZT is antagonist of stavudine.AZT is antagonist of stavudine.
LamivudineLamivudine – this deoxycitidine analogue is– this deoxycitidine analogue is
phosphorylated intracellularly inhibiting viral reversephosphorylated intracellularly inhibiting viral reverse
transcriptase & Hepatitis B virus polymerase. Astranscriptase & Hepatitis B virus polymerase. As
effective as AZT.effective as AZT.
AbacavirAbacavir - guanosine analogue, potent drug ,- guanosine analogue, potent drug ,
resistance development is slow. More toxic ( evenresistance development is slow. More toxic ( even
few fatalities are known )few fatalities are known )
124. Non-nucleoside reverse transcriptase inhibitors(NNRTI)Non-nucleoside reverse transcriptase inhibitors(NNRTI)
Nevirapine & Efavirenz – nucleoside unrelatedNevirapine & Efavirenz – nucleoside unrelated
compounds which directly inhibit reversecompounds which directly inhibit reverse
transcriptase without intracellular phosphorylation.transcriptase without intracellular phosphorylation.
On HIV 1, they are more potent than AZT, but do notOn HIV 1, they are more potent than AZT, but do not
inhibit HIV 2.inhibit HIV 2.
Resistance development is by point mutation.Resistance development is by point mutation.
In combinations they successfully reduce HIV-RNAIn combinations they successfully reduce HIV-RNA
levels.levels.
* Nevirprine is highly hepatotoxic.* Nevirprine is highly hepatotoxic.
125. Nucleotide inhibitor ( NT )Nucleotide inhibitor ( NT )
TenofovirTenofovir -- Tenofovir is a derivative of adenosineTenofovir is a derivative of adenosine
5¢-monophosphate lacking a complete ribose ring5¢-monophosphate lacking a complete ribose ring
and is the only nucleotide analog currently marketedand is the only nucleotide analog currently marketed
for the treatment of HIV infection. Like lamivudine ,for the treatment of HIV infection. Like lamivudine ,
tenofovir is active against HIV-1, HIV-2, and HBV.tenofovir is active against HIV-1, HIV-2, and HBV.
It is phosphorylated by cellular kinases to its activeIt is phosphorylated by cellular kinases to its active
metabolite, tenofovir diphosphate. The intracellularmetabolite, tenofovir diphosphate. The intracellular
diphosphate is a competitive inhibitor of viral reversediphosphate is a competitive inhibitor of viral reverse
transcriptases and is incorporated into HIV DNA totranscriptases and is incorporated into HIV DNA to
cause chain termination because it has an incompletecause chain termination because it has an incomplete
ribose ring.ribose ring.
126. Retroviral protease inhibitors ( PI )Retroviral protease inhibitors ( PI )
Protease enzyme encoded by HIV virus producesProtease enzyme encoded by HIV virus produces
structural proteins & enzymes. They act at late step instructural proteins & enzymes. They act at late step in
HIV replication ( even reverse transcrip, production isHIV replication ( even reverse transcrip, production is
based on them)based on them)
Drugs block this Protease enzyme, interfere with itsDrugs block this Protease enzyme, interfere with its
cleavage function. They are more potent viruscleavage function. They are more potent virus
inhibitors than AZT.inhibitors than AZT.
Effective in both , newly infected & chronicallyEffective in both , newly infected & chronically
infected cells.infected cells.
Because of them HIV-infected cell producesBecause of them HIV-infected cell produces
immature non infectious viral progeny. ( furtherimmature non infectious viral progeny. ( further
rounds of infection are prevented )rounds of infection are prevented )
Indinavir, Nelfinavir, Ritonavir, Saquinavir LopinavirIndinavir, Nelfinavir, Ritonavir, Saquinavir Lopinavir
127. Fusion inhibitorFusion inhibitor
Enfuvertide – this HIV derived synthetic peptideEnfuvertide – this HIV derived synthetic peptide
binds to HIV 1 envelope glycoprotein (gp-41). Itbinds to HIV 1 envelope glycoprotein (gp-41). It
prevents fusion of virus & cell membrane. Cell entryprevents fusion of virus & cell membrane. Cell entry
of virus is blocked.of virus is blocked.
It is ineffective against HIV 2.( Envelope protien isIt is ineffective against HIV 2.( Envelope protien is
gp-36 )gp-36 )
Started only when other drugs ( Regimens ) fail.Started only when other drugs ( Regimens ) fail.
Fusion inhibitors are future drugs.Fusion inhibitors are future drugs.
129. I.- Acute attackI.- Acute attack
A. Supressive therapy-A. Supressive therapy-
1.Chloroquine phosphate – tab. of 250 mg (base 150 mg)1.Chloroquine phosphate – tab. of 250 mg (base 150 mg)
4 tabs. Stat , then 2 tabs. After 6 hrs. on day 14 tabs. Stat , then 2 tabs. After 6 hrs. on day 1
Then 1 Bid for next 2 days.Then 1 Bid for next 2 days.
2.Chloroquine phosphate – inj. 3 to 3.5mg / kg 6 hrly. IM.2.Chloroquine phosphate – inj. 3 to 3.5mg / kg 6 hrly. IM.
(IV- rarely used- myocardial depression & hypotension )(IV- rarely used- myocardial depression & hypotension )
3. Quinine – tab. Of 300 mg 2 tabs Tid for 3 days, then 23. Quinine – tab. Of 300 mg 2 tabs Tid for 3 days, then 2
tabs. Bid for next 4 to 7 days.tabs. Bid for next 4 to 7 days.
B. Radical cure ( prevention of relapse )B. Radical cure ( prevention of relapse )
1. Full course of chloroquine + Primaqiune 7.5 mg bid for1. Full course of chloroquine + Primaqiune 7.5 mg bid for
next 15 days. ( Starting on 4next 15 days. ( Starting on 4thth
day of treatment )day of treatment )
2. Artesunate (100mg bid on 12. Artesunate (100mg bid on 1stst
day. Then 50 mg bid for nextday. Then 50 mg bid for next
4 days )4 days )
130. 3. Artemether ( 80 mg bid for 3 days )3. Artemether ( 80 mg bid for 3 days )
4. Halofantrine ( 500 mg. 6 hrly. 3 doses are given )4. Halofantrine ( 500 mg. 6 hrly. 3 doses are given )
II. Cerebral malariaII. Cerebral malaria
1. Quinine hydrochloride – 20 mg. / kg in 500 ml of 5 % dextrose1. Quinine hydrochloride – 20 mg. / kg in 500 ml of 5 % dextrose
IV drip is run slowly ( risk of cardiac depression , arrythmias &IV drip is run slowly ( risk of cardiac depression , arrythmias &
sever HYOPGLYCEMIA.sever HYOPGLYCEMIA.
2. Chloroquine inj.- 200 mg in 5 % sol. IM 4 to 6 hrly.2. Chloroquine inj.- 200 mg in 5 % sol. IM 4 to 6 hrly.
3. Artesunate or Artemether3. Artesunate or Artemether
4. Halofantrine4. Halofantrine
( INSPITE OF PROPER TREATMENT 50 % MORTALITY IS( INSPITE OF PROPER TREATMENT 50 % MORTALITY IS
KNOWN )KNOWN )
131.
.. III. Chloroquine resistant malariaIII. Chloroquine resistant malaria
1.Quinine 600 mg. Tid + Doxycycline 100 mg bid.1.Quinine 600 mg. Tid + Doxycycline 100 mg bid.
For 8 to 10 days.For 8 to 10 days.
2. Artesunate 100 mg. Bid x 3 days. + Sulfadoxin 15002. Artesunate 100 mg. Bid x 3 days. + Sulfadoxin 1500
mg. & pyremethamine 75 mg. single dose.mg. & pyremethamine 75 mg. single dose.
3. Artesunate 100 mg. Bid x 3 days. + Mefloquine 7503. Artesunate 100 mg. Bid x 3 days. + Mefloquine 750
mg. on 2mg. on 2ndnd
day & 500 mg. on 3day & 500 mg. on 3rdrd
day.day.
4. Artemether 80 mg Bid + Lumefantrine 480 mg Bid x4. Artemether 80 mg Bid + Lumefantrine 480 mg Bid x
3 days3 days
