Basic principles of chemotherapy/ AMAs covers definition, history of AMAs development, principles of AMAs, problems associated with AMAs, failure of therapy with examples.
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Chronic toxicity
Genotoxicity,
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Biopharmaceutics is defined as the study of factors influencing the rate and amount of drug that reaches the systemic circulation and the use of this information to optimise the therapeutic efficacy of the drug products.
Sulfonamide (also called sulphonamide, sulfa drugs or sulpha drugs) is the basis of several groups of drugs. The original antibacterial sulfonamides are synthetic antimicrobial agents that contain the sulfonamide group.
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Following points are included;
Various Definitions:
Acute toxicity
Subacute toxicity
Chronic toxicity
Genotoxicity,
Carcinogenicity,
Teratogenicity
Mutagenicity
General principles of treatment of poisoning
Clinical symptoms and management of various poisoning conditions.
like Barbiturate poisoning, Morphinpoisoning, Organophosphoruspoisoning, Lead poisoning, mercury poisoning, Arsenin poisoning, And its specific antidote
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Basic principles of chemotherapy
1. Basic principles of chemotherapy
S. Parasuraman, M.Pharm., Ph.D.,
Senior Lecturer, Faculty of Pharmacy,
AIMST University
2. Chemotherapy
Chemotherapy: chemo + therapy
The use of drug (chemical entity/ substance derived form
microorganisms) with selective toxicity against infections/
viruses, bacteria, protozoa, fungi and helminthes is called as
chemotherapy.
3. Antibiotics and Antimicrobials
• Antibiotics: Antibiotics are substances produced by
microorganisms, which selectively suppress the growth of or
kill other microorganisms at very low concentration.
• Antimicrobials: (chemotherapeutic agent + Antibiotics)
Any substance of natural, synthetic or semisynthetic origin
which at low concentrations kill or inhibits the growth of
microorganisms but causes little or no host damage.
5. History of chemotherapy
Before Ehrlich’s period (till 1900)
• Chaulmoogra oil by Hindus in leprosy
• Cinchona bark for fever
• ‘Mouldy curd’ by chines on boils
• Mercury by Paracelsus for syphilis
Ehrlich’s period (1900 to 1930)
• Organometallic dye for treatment for cane
After Ehrlich’s period (1930 to till date)
• discovery of sulfonamide (Prontosil)
6. Timeline history of
chemotherapy development
1908- Discovery
1959- Antitumor
of Arsphenamine
antibiotics 2007- Target specific
Alexander Fleming 1928- screens
Penicillin 1958- Methotrexate
2005- Tyrosine kinase
1957- 5-Fluorouracil inhibitors
1951- Thiopurines 1997- Monoclonal
antibody approved
Paul for the treatment of
1948- Anitfolates
Ehrilich tumor.
Father of Gerhard Domagk 1939-
Sulfonamidochrysoidine 1944- Waksman et 1963-
Chemotherapy 1996- Imatinib
(Prontosil) al., discovered Vinca alkaloids
streptomycin.
1962- nalidixic acid
1900- Paul 1943- Nitrogen
Ehrilich mustard in
Chemotherapy 1932- Prontosil- lymphomas 1963 to 1970-
Animal model First sulfonamide- Treatment for
developed Bayer’s Laboratory Hodgkin’s disease
1900 1960 1980 2015
1920 1940
8. Principles of antimicrobial therapy
• Diagnosis: Site of infection, responsible organism,
sensitivity of drug
• Decide- chemotherapy is necessary: Acute
infection require chemotherapy whilst chronic infections
may not. The chronic abscess respond poorly, although
chemotherapy cover is essential if surgery is undertaken
to avoid a flare-up of infection.
• Select the drug: Specificity (spectrum of activity,
antimicrobial activity of drug), pharmacokinetic factors
(physiochemical properties of the drug) , patient related
factors (allergy, renal disease)
9. Principles of antimicrobial therapy
Cont.,
• Frequency and duration of drug administration: Inadequate
dose may develop resistance, intermediate dose may not cure
infection, optimize dose should be used for therapy.
• Continue therapy: Acute infection treated for 5-10 days. But some
of the bacterial infection exceptions to this. E.g.: Typhoid fever,
tuberculosis and infective endocarditis (after clinical cure, the therapy
is continued to avoid relapse).
• Test for cure: After therapy, symptoms and signs may disappear
before pathogen eradicated.
• Prophylactic chemotherapy: To avoid surgical site infections.
11. Classification of antimicrobials
A. Chemical structure
B. Mechanism of action
C. Type of organisms (against which primarily active)
D. Spectrum of activity
E. Type of action (bacteriostatic and bactericidal)
F. Source of antibiotics
14. B. Mechanism of action
cell membrane
THFA
Ribosomes
PABA
DNA gyrase
metabolism
protein
synthesis
Cell wall synthesis m-RNA code
15. B. Mechanism of action
Cont.,
Leakage form
cell membrane
Polypeptides- Polymyxines,
colistin. Inhibition of Cell
Polyenes- Amphotericin B, Membrane
Nystatin, Hamycin Fluoroquinolones
THFA Rifampin
Ribosomes
Inhibition of
PABA
metabolism Inhibition of DNA
Sulfonamides gyrase
Sulfones
Trimethoprim Fluoroquinolones
PAS Inhibition of
Pyrimethamine Cell wall synthesis
Ethumbutol Beta-lactams
Misreading of Inhibition of
Cephalosporins m-RNA code protein
Vancomycin synthesis
Aminoglycosides- Tetracyclines
Streptomycin, Aminoglycosides
Gentamicin Macrolides
Clindamycin
Chloramphenicol
16. C. Type of organisms (against which primarily active)
• Antibacterial: Penicillins, Aminoglycosides, Erythromycin,
etc.
• Antiviral: Acyclovir, Amantadine B, Zidovudine, etc.
• Antifungal: Griseofulvin, Amphotericin B, Ketoconazole, etc.
• Antiprotozoal: Chloroquine, Pyrimethamine, Metronidazole,
etc.
• Anthelminthic: Mebendazole, Niclosamide, Diethyl
carbamazine, etc.
17. D. Spectrum of activity
Narrow-spectrum Broad-spectrum
Penicillin G, Streptomycin, Tetracyclines,
Erythromycin Chloramphenicol
effective against specific effective against a wide
type of bacteria range of bacteria,
either gram-positive or both gram-positive and
gram-negative gram-negative
18. D. Type of action
(bacteriostatic and bactericidal)
Bacteriostatic:
Inhibit the growth of Bacteria.
E.g.: Sulfonamides, Tetracyclines,
Chloramphenicol, Erythromycin,
Ethambutol
Bactericidal:
Kill the microbes.
E.g.: Penicillins, Aminoglycosides,
Polypeptides, Rifampin, Isoniazid, Note: Some b’static drugs may act
Vancomycin, Ciprofloxacin, Metronidazole, b’cidal at high concentration
Cotrimoxazole (Sulfonamides, nitrofurantion)
20. Hypersensitivity
reaction
Drug
Toxicity resistance
Problems with AMAs
Drug tolerant
Superinfection
21. Toxicity
Local irritancy:
• exerted site of administration. E.g.: Gastric irritation, pain and
abscess formation at the site of i.m. inection,
thrombophlebitis of injected vein.
Systemic toxicity:
• Dose related organ damage.
– High therapeutic index agents may not damage host cells, E.g.:
penicillin, erythromycin.
22. Toxicity
Cont.,
Systemic toxicity:
• The agent which have low therapeutic index exhibits more toxicity.
E.g.:,
aminoglycosides tetracycline chloramphenicol
(renal and CNS toxicity) (liver and renal toxicity) (bone marrow depression)
23. Toxicity
Cont.,
Systemic toxicity:
• Very low therapeutic index drug is used when no suitable
alternative AMAs available,
• E.g.: Vancomycin
(hearing loss, kidney damage,
“red man’ syndrome)
• polymyxin B
(neurological and renal toxicity)
Vancomycin toxicity
24. Hypersensitivity reaction
• All AMAs are capable to causing hypersensitive reaction, and
this this reactions are unpredictable and unrelated to dose.
E.g.: Penicillin induced anaphylactic shock (prick skin testing)
To avoid
Inj. Penicillin induced Perform sensitivity test before
anaphylactic shock administering penicillin Inj.
25. Resistance
• Unresponsiveness of a microorganism to an AMA, and is
similar to the phenomenon of drug tolerance.
– Natural resistance
– Acquired resistance
• Natural resistance: Some microbes have resistant to
certain AMAs. E.g.: Gram negative bacilli not affected by
penicillin G; M. tuberculosis insensitive to tetracyclines.
• Acquired resistance: Development of resistance by an
organism (which was sensitive before) due to the use of
AMA over a period of time. E.g.: Staphylococci, tubercle
bacilli develop resistance to penicillin (widespread use for
>50 yr). Gonococci quickly developed resistant to
sulfonamides in 30 yr.
26. Resistance
Cont.,
Development of resistance
• Resistance mainly developed by mutation or gene transfer.
• Mutation: Resistance developed by mutation is stable and
heritable genetic changes that occurs spontaneously and
randomly among microorganism (usually on plasmids).
• Mutation resistance may be single step or multistep.
– Single gene mutation may confer high degree of resistance. E.g.:
enterococci to streptomycin
– Multistep mutation may modify the more number of gene that will
decreases the sensitivity of AMAs to pathogens.
27. Resistance
Cont.,
• Development of resistance
• Gene transfer (Infectious resistance): From one organism to
another organism.
– Conjugation
– Transduction
– Transformation
a a
a a
b b
Transposon Plasmid b b
donor cointegrate
Transfer of resistance genetic elements within the bacterium
28. Resistance
Cont.,
Development of resistance
Gene transfer - Conjugation:
• cell-to-cell contact; transfer of chromosomal or
extrachromosomal DNA from one bacterium to
another through sex pili. The gene carrying the
resistance or ‘R’ factor is transferred only if another
“resistance transfer factor” (RTF) is present. This will
frequently occurs in gram negative bacilli.
• The nonpathogenic organisms may transfer ‘R’ factor
to pathogenic organisms, which may become wide
spread by contamination of food and water.
• The multidrug resistance has occurred by
conjugation.
– Chloramphenicol resistance to typhoid bacilli
– Penicillin resistance to Haemophilus, gonococci
– Streptomycin resistance to E.coli
29. Resistance
Cont.,
Development of resistance Gene
transfer- Transduction:
• Transfer resistance gene through
bacteriophage (bacterial virus) to
another bacteria of same
species.
– E.g.: Transmission of resistance
gene between strains of
staphylococci and between strains
of streptococci.
30. Resistance
Cont.,
Development of resistance
Gene transfer - Transformation:
• It will occur in natural conditions.
• Bacteria taking up naked DNA form its environment and
incorporating it into its genome through the normal cross-
over mechanism.
31. Drug Tolerant
• Loss of affinity of target biomolecule of the microorganism
with particular AMAs, E.g.: Penicillin resistance to
Pneumococcal strain (alteration of penicillin binding proteins)
Drug target site Change in protein
configuration- loss of
affinity
32. Superinfection (Suprainfection)
• A new infection occurring in a patient having a
preexisting infection. Superinfections are most
difficult to treat.
33. Superinfection
Cont.,
• Development of superinfection associated with the use of
broad/ extended-spectrum of antibiotics, such as
tetracyclines, chloramphenicol, ampicillin and newer
cephalosporins.
• Superinfections are more common when host defence is
compromised.
• Superinfections are generally most difficult to treat.
– bacterial superinfection in viral respiratory disease
– infection of a chronic hepatitis B carrier with hepatitis D virus
– Piperacillin-tazobactam may cause superinfection with candida
34. Superinfection
Cont.,
• Treatment for superinfection
– Candida albicans: Monilial diarrhoea, Candidal vulvovaginitis or vaginal thrush
(an infection of the vagina's mucous membranes) treat with nystain or
clotrimazole
– Resistant Staphylococci: treat with coxacillin or its congeners
– Pseudomonas: Urinary tract infection, treat with carbenicillin, piperacillin or
gentamicin.
• Superinfections minimized by
– using specific (narrow-spectrum) AMA (whenever possible)
– avoid using (do not use) antimicrobials to treat self limiting or untreatable
(viral) infection
– avoid prolong antimicrobial therapy.
35. Choice of an antimicrobial agents
Patient related factors
Drug factors
Organism-related considerations
36. Choice of an antimicrobial agents
Patient related factors:
• Patient age (chloramphenicol produce gray baby syndrome in
newborn; Tetracyclines deposition in teeth and bone-below
the age of 6 years)
• Renal and hepatic function (aminoglycoside, vancomycin-
renal failure; erythromycin, tetracycline- liver failure)
• Drug allergy (History of known AMAs allergy should be
obtained) .
– Syphilis patient allergic to penicillin – drug of choice is tetracycline
– Fluoroquinolones cause erythema multiforme
• Impaired host defence
37. Choice of an antimicrobial agents
Cont.,
Drug factor:
• Pregnancy
– All AMAs should be avoided in the pregnant
– many cephalosporins and erythromycin are safe, while safety data on
most others is not available.
• Genetic factors
– Primaquine, sulfonamide fluoroquinolones likely to produce
haemolysis in G-6-PD deficient patient)
38. Choice of an antimicrobial agents
Cont.,
Organism-related considerations:
• A clinical diagnosis should first be made, and the choice of the
AMAs selected
• Clinical diagnosis itself directs choice of the AMA
• Choice to be based on bacteriological examination
(Bacteriological sensitivity testing)
39. Choice of an antimicrobial agents
Cont.,
Drug factor:
• Spectrum of activity (Narrow/ broad spectrum)
• Type of activity
• Sensitivity o f the organism (MIC)
• Relative toxicity
• Pharmacokinetic profile
• Route of administration
• Cost
41. Combined use of antimicrobials
• To achieve synergism, Rifampin+ isoniazid for tuberculosis
•
• To reduce severity or incidence of adverse effects,
Amphotericin B + rifampin (rifampin enhance the antifungal
activity of amphotericin B)
• To prevent resistance (Concomitant administration of
rifampin and ciprofloxacin prevents Staph. aureus
resistance ciprofloxacin)
• To broaden the spectrum of antimicrobial action
(cotrimoxazole: Trimethoprim/sulfamethoxazole)
43. Prophylactic use of antimicrobials
• Prophylaxis against specific organisms (Cholera: tetracycline
prophylaxis; Malaria: for travelers to endemic area may
take chloroquine/ mefloquine)
• Prevention of infection in high risk situations
• Prophylaxis of surgical site infection
• Prophylaxis against specific organisms
• Prevention of infection in high risk situations
• Prophylaxis of surgical site infection
45. Failure of antimicrobial therapy
• Improper selection of AMAs, dose, route or duration of
treatment.
• Treatment begun too late
• Failure to take necessary adjuvant measures
• Poor host defence
• Trying to treat untreatable (viral) infections
• Presence of dormant or altered organisms which later give
risk to a relapse
46. Common side effects with
chemotherapeutics agents
Think before dispensing
Thank U
Editor's Notes
Paul Ehrilich dies: father of chemotherapyImatinib is a Bcr-Abl tyrosine kinase inhibitor for the treatment of chronic myelocytic leukemia