Sulfonamides Flashcards
SULFONAMIDES
The stain sulfonamide is a generic name for derivatives of _________________ (____________).
para aminobenzene sulfonamide
sulfanilamide
para aminobenzene sulfonamide (sulfanilamide) was the 1st effective chemotherapeutic agent to be employd systemically for the prevention and cure of bacterial infections in man.
T/F
T
SULFONAMIDES
para aminobenzene sulfonamide (sulfanilamide) were the main stay of antibacterial chemotherapy before the __________ become genrally available.
penicillin
SULFONAMIDES
Most of them are relatively (soluble or insoluble ?) in H2O but their sodium salts are readily (soluble or insoluble?) .
Insoluble
Soluble
SULFONAMIDES
Conc of sulfonamides in body fluids are determined by ________ rather than by _______.
chemical techinicals
bioassay
SULFONAMIDES
The minimal structural prerequisites for antibacterial action are in __________________.
The ______________ is not essential as such, but the important feature is that the _________________ is ________________.
sulfanilamide itself
SO2 NH2 gaps
sulfur is directly linked to the benzene ring
SULFONAMIDES
The para-__________ is essential.
NH2gp (N4)
SULFONAMIDES
_______ of the para –_____ abolishes in-vitro activity; but _______ may occur in vivo with a resulting _________
Acylation
NH2
deacylation
return of potency.
SULFONAMIDES
EFFECTS ON MICROBIAL AGENTS
Effective against gram ____________________ microorganisms, they are generally Bacterio________ .
both gram – positive & gram negative
static
SULFONAMIDES
MECHANISM OF ACTION
Sulfonamides are __________ and _______ of ________ and prevent normal bacteria
utilization of it for synthesis of ________________, ploA (Folic acid).
structural analogues and competitive antagonists
PABA
pteroy/glutanic acid
SULFONAMIDES
MECHANISM OF ACTION
Suphonamides are (competitive or non-competitive?) inhibitors of the bactieral enzyme responsible for the _______ of _______ into ____________
competitive
incorporation of PABA
dihydropletroci acid
dihydropletroic acid is the immediate precursor of ________
folic acid.
____________ is the immediate precursor of folic acid.
dihydropletroic acid
SULFONAMIDES
Sensitive microorganisms are those that _______________, bacteria that can ______________ are not affected.
must synthesize their own PHA
utilize proformed PGA
Bacterio______ induced by sulfonamides is counter acted by ______ (competitively or non-competitively?)
stasis
PABA
competitively
sulfonamides
Trimethoprim exerts _____ effect with sulfonamides, it is a potent & selective competitive inhibitor of _________
synergistic
dihydrofolate reductase
Trimethoprim - inhibitor of dihydrofolate reductase
dihydrofolate reductase Reduces _______ to _________ which is required for _________ reactions, hence sequential blockage.
dihydrofolate
tetralydrofolate
one-carbon transfer
Antagonists of sulfonamide are ———-, ___________ e.g. _______
PABA
local anesthetic
procain
procaine is an ______ of _______
ester of PABA
sulfonamides
Mech of resistance, an altered enzymatic constitution of the _____________ bs(i) an alteration in the _______ that ______ ———-
2) an increased capacity to _______ or ___________
(3) an alternative __________ for ____________
4) an increased production of _________ or ____________
bacterial cell
enzyme that utilizes PABA,
destroy or inactivate the drug
metabolic pathway for synthesis of an essential metabolite
an essential metabolite or drug antagonist.
ABSORPTION, FATE & EXCRETION of sulfonamides
•It is rapidly absorbed for ______% of an oral dose except for those _____________.
•In urine ______ after a ingestion, variable & unreliable absorbtion from ______,_______,———
70 – 100
designed for their local effect in the GIT
30 mins
vagina, respiratory track, abraded skin.
All sulfonamides are bound to _______ in variable degree particularly _______.
plasma protein
albumin
Sulfonamides are distributed throughout _____ tissues and readily _______,______, and _________ fluid up to 50-80% of the simultaneously determined concentration in blood
all
outer pleural peritoneal , synovial, ocular
Sulfonamides readily attain concentration in foetal tissues sufficient to cause _______________________
both antibacterial and toxic effects
Sulfonamides
The metabolic product, the _______ forms have _____ antibacterial activity but are ________ compared to the ___________ form.
acetylated
no
equally toxic
un acetylated
acetylation of sulfonamides is a function of ________ function and time
hepatic
Sulfonamides
__________ is a major factor of excretion of both the acettlated and unacetylated form
The rate of excretion ____eases as their pKA ____eases . Tubular reabsorption and secretion also play their role
Glomerular filtration
incr; decr
Sulfilsoxazole diolamine in 4% solution or ointment for ______ use in the ____.
Sulfamethoxazole – precautions to avoid ________ because of high % of _______, relatively (soluble or insoluble?) form in the urine.
topical; eye
crystallnurial; acetylated ; insoluble
Sulfadiazine – _________ urine to decrease tubular reabsorption and increase renal clearance.
Sulfasalazine – used in _________ and _______ but recurrence in 1/3 of patients, 1 to 3g dly.
Alkalinize
ulcerative colitis & regional enlevitis
___________ in 4% solution or ointment for topical use in the eye.
___________– precautions to avoid crystallnurial b/c of high % of acetylated, relatively insoluble form in the uiwine.
Sulfilsoxazole diolamine
Sulfamethoxazole
Sulfasalazine – There is evidence that it alters the intestinal microflra of persons with ulcerative colitis.
T/F
F
There is no evidence that it alters the intestinal microflra of persons with ulcerative colitis.
Sulfacetamide.
It is the ____ - _______ – sublitered derivative
•aqueous solubility (1:140) is 90* that of _________.
• Used in _________ infections.
N1 – a cetyl
sulfadiazine
opththalmic
Silver sulfadiazine to silver is released (slowly or rapidly?) from the prep in concentrations that are ________ to the microorganism.
•Little ______ is absorbed but _______ concentration may reach toxic levels.
•It is used to decrease microbial colonization &incidence of infections of _______ from ______
Slowly
selectively toxic
Silver ; sulfadiazine
wounds from burns.
_________ is used to decrease microbial colonization &incidence of infections of wounds from burns.
Silver sulfadiazine
The trimethoprim- Sulfamethoxazole combination ( ____________)
•Trimethoprim is a ____________.
•Trimethoprim is __________times more potent than Sulfamethoxazole and effective against gram positive and negative microorganisms although resistance can occur if used alone.
co-trimoxazole
di-amino pyridine
20 to 100
The trimethoprim- Sulfamethoxazole combination
Which is more potent, Trimethoprim or
Sulfamethoxazole
Trimethoprim is 20 to 100 times more potent than Sulfamethoxazole and effective against gram positive and negative microorganisms although resistance can occur if used alone.
The trimethoprim- Sulfamethoxazole combination ( co-trimoxazole)
the most efficient ratio against the greatest number of microorganisms is ____ parts Sulfamethoxazole to ___ part trimethoprim
20
One
The trimethoprim- Sulfamethoxazole combination
The combination is bacterio____ for some organisms .
Resistance formation is (lower or higher?) than to either substances alone
cidal
Lower
The combination(co-trimoxazole ) appears to ______ the absorption of ________,
PPC of trimethoprim in ______ while sulfamethoxazole takes _______
slow down
sulfamethoxazole
2 hours; 4 hours
Sulphonamides therapy is useful in the following cases
-______
-_________
-_________
-_______
UTI
Bacillary Dysentary
Meningococcal
Nocardiosis
- Meningococcal :
N.meningitidis Rx now with ________,________, or _________ ( _________ for some sensitive strains) because of ____________ to sulfonamides except if ———— to sulfonamides
Penicillin or ampicillion or Cephalosporins
chloramphenicol
resistance formation
sensitivity
PRINCIPLE OF UTI DRUG TREATMENT
Pylonephitis + Bacteremia/septiceamia= ___________, __________.
________ (or other quinolones) or other drugs to which the organisms are sensitive for example ________,_________etc
Amoxicill/clavulanic acid
cephalosporins
Ciprofloxacin
gentamicin, sulfonamides
PRINCIPLE OF UTI DRUG TREATMENT
____________+ ________/________= Amoxicill/clavulanic acid,
cephalosporins. Ciprofloxacin(or other quinolones) or other drugs to which the organisms are sensitive for example gentamicin, sulfonamides etc
Pylonephitis
Bacteremia/septiceamia
PRINCIPLE OF UTI DRUG TREATMENT
Mixture of microorganism of organisms can occur also, then sulfonamide may be useful as ________________ when indicated
a co- administered drug
PRINCIPLE OF UTI DRUG TREATMENT
_________/________ (Re-infectioin or Bacteraemia) in some cases may justify the use of sulfonamides
Chronic /Recurrent
PRINCIPLE OF UTI DRUG TREATMENT
CHRONIC OR RECURRENT CAN BE CAUSED BY __________,______________ , ABNORMALITY OF ______, _________ AND __________
Urolithiasis/Nephrolithiasis,
Obstruction
TRACT, DIABETES
DECREASED URINATION
PRINCIPLE OF UTI DRUG TREATMENT
Acute Lower tract INFECTION: pending sensitivity
_____________
__________ especially in pregnancy, for nonpregnant, quinolones, sulfonamide, genticin also when indicated.
Amoxicillin/clavulanic acid
cephalosporins
Methenamine – URINARY tract antiseptic owes it activity to ________.
____________ of urine promotes its antibacterial action.
formaldehyde
Acidification
Methenamine –
________ decomposes in the blood & tissues so no ___________ from aminoria or formaldelyde.
Various substances given in addition to keep urine pH _______ e.g _______,_______,_______
So little; systemic toxicity
below 5.5
Ascorbic acid, mandelic, lippuric acid.
Methenamine –
is a primary drug for UTI
is a secondary drug for chronic suppressive Rx.
T/F
F
F
is not a primary drugs for UTI but for chronic suppressive Rx.
Microorganisms develop resistance to formaldehyde.
T/F
F
Microorganisms do not develop resistance to formaldehyde.
The Quinolones: This & _________ inhibit ________ during bacteria replication.
Nalidixic acid
DNA synthesis
Nalidixic acid is bacteri_____ to most gram-negative bacteria in UTI.
cidal
Nalidixic acid :
(Poorly or Well?) absorbed from GIT
(high or low ?) conc of Nalidixic acid & metabolite (hydroxynalidixic acid) in urine.
_______ and _______ are necessary if Treatment last longer than 2 weeks.
Well
High
LFT & blood tests
Nalidixic acid :
ADRs include ____ toxicity, ____ disturbances occasionally
CNS
GIT
Which is more potent, oxolinic acid or nalidixic acid.
Oxolinic acid 2 to 4 x more potent than nalidixic acid.
Norfloxacin, ciprofloxacin & perfloxacin good activities against gram-positive and negative orgs.
Norfloxacin, ciprofloxacin & perfloxacin can be used for systemic diseases.
T/F
T
T
________ acid similar in structure to oxolinic acid.
Cinoxacin
Nitrofuratoin.
It is a ( natural or synthetic ?) nitrofuran in prevention & treatment of UTI.
It is bacteri______ for most susceptible microorganisms at conc of 32 ug/ml or less.
(Poorly or Well?) absorbed from GIT.
_________ing urine decreases antibacterial activity
synthetic; ostatic
Well; Alkalinizing
Nitrofuratoin.
Side effects
Nausea, vomiting and diarrhoea.
_________ is uncommon but a serious side effect.
Chronic active hepatitis
Phenazopyridine HCl – is not a ________ but ________ on the urinary tract & alleviates _____ and _________ (irritation induced)
urinary antiseptic
an analgesic
dysuria; frequency of urination
Phenazopyridine HCl
It colors the urine _______ or _______.
GIT upset in ____% of patients.
orange or red
10
Phenazopyridine HCl .
Combination available with __________ and _________
sulfisoxazole & sulfamethoxazole.
SULPHONES
They are derivatives of ___________________________________ (dapsone, DDS), all of which have certain __________ in commons.
They are related chemically to the ———————. E.g. _______ and _______
4, 4-diaminodiphenylsulfone
pharm properties
sulfonamides
Dapsone & sulfoxone sodium.
much of action of sulphones are similar to sulfonamides.
T/F
T
SULPHONES
Secondary resistance can occur to Dapsone by ______ especialy __________ particularly with _____ drug therapy.
Primary resistance also occurs which can be ______________
M leprae; lepromatous leprosy; single
partial or complete
SULPHONES
UE – ________ is commonest. ___________ deficiency predisposes to _______.
______________ is also common.
Hemolysis
Glucose-6-P04 dehydrogenese
hemolysis
Methemoglobineria
SULPHONES
UE –
Anorexia, nausea & vomiting, CNS manifestation, exacerbation of lemomatous leprosy “ __________ ” 5 to 6/52 after start therapy in malnourished people.
________ of treatment may be necessary in the course of treatment
sulfone syndrome
Stoppage
Dapsone is (slowly or rapidly?) and almost ________ absorbed from the GIT.
Slowly
completely
Sulfoxone is (completely or incompletely ?) absorbed from GIT & (small or large?) amount are excreted in feces.
Incompletely; large
DAPSONE
A total of ____% of Dapsone is bound to plasma potency.
It is retain in _______ and ______.
They are retained in the circulation for a (short or long?) time because of ______________________ hence __________________ is advisable.
70
skin and muscle
Long ; intestinal reabsorption from the bile
periodic interruption of treatment
Dapsone is ______ in the line & then is genetically determined
acetylated
DAPSONE
Dosage: treatment with Dapsone is usually started with (small or large?) amounts & increase, when serious gastric irritation occurs, ________ is given instead.
small
sulfoxae Na
Sulfones are active against P. faciparium
T/F
T
Sulfones are active against P. faciparium even used in P falciparium resistant cases combined with __________.
pyrimethamine
