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ANTIBIOTICS Flashcards

ANTIBIOTICS

1
Q

Basic Structure of Penicillins?

A

Thiazolidine ring, which is attached to Beta-lactam ring and the Beta-lacatam ring is attached to Side chain

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2
Q

All the Pc derived from 6-APA method are all advantageous over PcG how???

A

Improved antibacterial activity
greater stability against Beta-lactamases
better pharmacokinetic properties

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3
Q

Are Pc bactericidal or bacteriostatic?

A

Bactericidal

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4
Q

MOA of Pc?
Function of the peptidoglycan component?
3 parts of Peptidoglycan?

A

Inhibit the development of the cell wall.

Peptidoglycan is a major component in the bacteria cell wall and it provides rigidity due to the cross linked structures. Cell wall is rigid structure and prevents the bacteria from brusting due to osmotic flow.

The 3 parts are N-Acetylglucosamine (NAG),
N-Acetylmuramic acid (NAM) and the cross linking of the 3rd AA (lys) of the pentapeptide (NAM) to the 4th AA (ala) of the opposite NAM by the 5 glycine aa.

lysine for G +ve and Meso-diaminopimelic acid for G - ve

Cross linking is done by transpeptidase (Pc inhibits this). Thus B-lactams inhibit the cross linking of peptidoglycans via inhibiting trranspeptidation and stimulation of autolysins that break down cell wall. this causes disruption of synthesis of the cell wall and promote its active destruction.

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5
Q

What are the narrow spectrum Pc?

A

Benzylpenicillin
Procaine penicillin
Benzathine penicillin
Phenoxymethlypenicillin

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6
Q

What are the narrow spectrum Pc with Anti-Staph?

A

Dicloxacillin and flucloxacillin

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7
Q

What are the moderate spectrum Pc?

A

Ampicillin and amoxicillin

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8
Q

What are the broad spectrum Pc?

A

Amoxicillin with Clavulanic acid

Piperacillin with Tazobactam

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9
Q

What are spectrum of activity of Pc?

A

highly active against Gram +ve (bacillus anthracis, clostridium perfringens)

some Gram - ve, spirochaetes and Actinomycetes

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10
Q

What is distribution of PcG?

A

Doesn’t enter the CSF when meninges are normal but when inflamed, Pc penetrates and is actively transported out, thus given with probenecid to prevent this.`

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11
Q

What are the indications for PcG?

A 
Endocarditis, 
Syphilis,
 CAP, 
Aspiration Pneumonia, 
Meningitis and 
Septicaemia
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12
Q

Dosage for PcG?

A

0.6g - 1.2g (IV) every 4 - 6 hrs. not oral because acid destroys the PcG

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13
Q

Indications for procaine pencillins?

A

Respiratory tract infections, syphilis and cellulitis and erysipelas

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14
Q

dosage for procaine penicillins?

A

1g - 1.5g once daily and IM

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15
Q

Pk of procaine penicillins?

A

given IM and Absorbed slowly into circulation and hydrolysed into PcG and maintain conc upto 12 to 24 hrs

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16
Q

Pk for benzathine penicillins?

A

given IM and absorbed slowly into circulation and hydrolysed to PcG upto 4 weeks

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17
Q

Indications for Benzathine penicillins?

A

Prevention of rheumatic fever, which usually follows a streptococcus pyogenes
Early and Latent syphilis

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18
Q

Dosage for benzathine Pc?

A

0.9 - 1.8 g IM

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19
Q

Pk of PcV?

A

more stable in acidic medium (thus oral)
completely absorbed in the GIT
Rapid absorbed

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20
Q

Indications for PcV?

A

s.pyogenes tonsilitis/ pharyngitis or skin infections
prevention of rheumatic fever
gingivitis (with metronidazole)

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21
Q

Dosage for PcV?

A

250 to 500 mg every 6 to 8 hrs

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22
Q

Spectrum of dicloxacillin and flucloxacillin?

A

resistant to beta lactamase produced by staphylococci but no activity against MRSA

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23
Q

Pk of Dicloxacillin and Flucloxacillin?

A

absorption is reduced by presence of food in the stomach. only orally

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24
Q

Indications for dicloxacillin and flucloxacillin?

A 
Pneumonia
Osteomyelitis 
septicaemia 
endocarditis 
surgical prophylaxis 
staphylococcal skin infections
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25
Q

Adverse effects of dicloxacillin and flucloxacillin?

A

Increase in liver enzymes and bilirubin
flucloxacillin –> severe hepatic reactions
dicloxacillin –> interstital nephritis

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26
Q

Indications for Moderate spectrum Pc?

A 
Chronic bronchitis 
CAP
Otitis media 
Gonococcal infection 
Epididymo orchitis 
non-surgical prophylaxis of endocarditis 
acute cholecystitis
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27
Q

Pk for moderate spectrum Pc?

A

ampicillin–> only available as IV, 1 hr half life and low peak plasma conc

amoxicillin –> absorbed more rapidly and completely from GIT, high peak plasma conc (2 times)

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28
Q

dosage for moderate spectrum Pc?

A

ampicillin –> 500 mg - 1 g IV 4-6 hrs

amoxicillin –> 250 -500 mg every 8 hrs or 1 g bd

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29
Q

Indications for amoxicillin & clavulanic acid?

A 
HAP
PID
UTI
Epididymo orchitis 
Bites and fist injuries
Otitis media 
sinusitis 
cholecystitis
melioidosis
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30
Q

indications for piperacillin with tazobactam

A

Activity against pseudomonas aeruginosa

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31
Q

Resistance to Pc

A

Via destruction of AB by beta-lactamase enzymes - antibiotic cleaving.
beta-lactamases catalyse the hydrolysis of the beta lactam ring. thus breaking the ring structure (amide bond) and decrease in AB activity and no longer inhibit cell wall synthesis. penicillin to penicilloic acid by penicillinase.

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32
Q

ambler classification of beta lactamases

A 
Class A: inhibited by clavulanic acid. Serine based (a, c ,d). Pc , ceph and monobactam 
Class b is zinc based
Class c 
Class d 
Clavulanic acid doesn't inhibit b,c,d
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33
Q

How do B-lactamases inhibitors work?

A

The molecules inactivate b-lactamase enzymes because they have a similar structure of B-lactam ring as Pc. thus binds to B-lactamases and protects hydrolyzable penicillins from inactivation

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34
Q

Adverse effects of penicillins?

A

Hypersensitivity
Serum sickness: fever, lymphadenopathy, oedema and rash
SJS
Angioedema: swelling of face, tongue and lips
Allergic reaction

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35
Q

Monobactam drugs?

Spectrum?

A

Aztreonam (narrow spectrum)
Bactericidal
active against g-ve and aerobic g -ve (b-lactamase producing H.influenzae and pseudomonas spp

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36
Q

Indications for Aztreonam

A

Infections caused by G -ve aerobes
septicaemia
lower RTI
Pseudomonas Aeruginosa –> cystic fibrosis
people with severe hypersensitivity to Pc

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37
Q

MOA of Aztreonam

A

inhibits cell wall synthesis by binding to PBP-3 of G -ve

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38
Q

Carbapenems drugs?

A

Imipenem, Ertapenem and Meropenem

Broadest spectrum –> good activity against g +ve, g -ve & anaerobes

all are activity against staph aureus (no MRSA) and bacteroides fragilis

only Imipenem and meropenem is active against pseudomonas aeruginosa

ertapenem is inactive agianst p.aeruginosa and acinetobacter

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39
Q

Indications for ertapenem, imipenem and meropenem

A

ertapenem: community acquired infections

Imipenem & meropenem: UTI, Lower RTI and intre-abdominal infections

Meropenem as lower incidence of seizures thus tx for meningitis and melioidosis

Imipenem for nosocomal infections and life threatening multi resistant gram -ve infections

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40
Q

What the 1st generation cephalosorins and adverse effects

A

cefalexin (oral)
cefazolin (inj)
cefalotin (inj)

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41
Q

What the 2nd generation cephalosorins and adverse effects

A

Cefoxitin (inj) –> serum sickness like syndrome in children - cefuroxime is preferred
Cefaclor (oral)
Cefuroxime (oral)

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42
Q

What the 3rd generation cephalosorins and adverse effects

A

Cefotaxime (inj) -> life threatening arrhythmias with rapid infusion
Ceftriaxone (inj) -> pseudolithiasis & nephrolithiasis due to calcium ceftriaxone complex
ceftazidime (inj)

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43
Q

What the 4th generation cephalosorins

A

cefepime (inj)

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44
Q

Others for cephalosorins

A

ceftraoline (inj)

ceftobiprole

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45
Q

Antipseudomonal Cephalosorins

A

ceftazidime
ceftolozane with tazobactam
cefepime

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46
Q

Anti MRSA cephalosorins

A

Ceftaroline

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47
Q

Pk for cephalosporins

A

poor absorptions from GIT thus IV preferred
1st and 2 nd are not used for meningitis, poor csf
3rd and 4th are good csf penetration

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48
Q

spectrum for cephalosporins

A

1st excellent g +ve and modest g -ve
2nd better activity against g -ve
3rd activity against g +ve and enterobacteriaceae & pseudomonas aeruginosa
4th increased stability to hydrolysis by b-lactamases

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49
Q

Indications of 1st cephalosporins

A

all are used in staph & strep fx in Pc allergy people and UTI

addition cefazolin –> surgical prophylaxis

cefalexin –> epididymo orchitis

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50
Q

Indications for 2nd cephalosporins

A

cefaclor -> otitis media
RTI by H.influenzae
Sinusitis

Cefuroxime -> Otitis media
RTI by H. influenzae
Sinusitis
Gonococcal infection

Cefoxitin -> Alternative combination for surgical prophylaxis and anaerobic infections

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51
Q

indications for 3rd cephalosporins

A

Cefotaxime: empirical tx of bacterial meningitis

ceftraixone: used in Pc allergy and CI aminoglycosides
ceftazidime: tx of P.aeruginosa, melioidosis and empirical tx of sepsis in neutropenic or immunocompromised people

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52
Q

Indications for 4th cephalosporins

A

P.aeruginosa infections

empirical tx of sepsis in neutropenic or immunocompromised people

Fx caused by mo resistant to other cephalosporins

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53
Q

Pk for ceftaroline

A

ceftaroline fosamil is inactive produrg and is given IV and rapidly biotransformed into active ceftaroline by phosphatases

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54
Q

indication for ceftaroline

A

complicated skin and soft tissue infections

CAP

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55
Q

Adverse effects of cephalosporins

A

Neurotoxicity
bleeding
blood dyscrasias

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56
Q

Macrolides drugs

A

CARE

Clarithromycin
Azthromycin
Roxithromycin
Erythromycin

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57
Q

what drug is used against macrolide resistant strains

A

Telithromycin with is classified as Ketolides

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58
Q

MOA of Macrolides?

A

These are bacteriostatic AB

Inhibit protein synthesis by binding reversibly to the 23s rRNA of the 50s Subunit. theis inhibits translocation step so the AA residing at the A site fails to move to P site and this prevents the release of tRNA after the peptide bond formation.

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59
Q

Spectrum of Macrolides

A

LMS CMC

L.pneumophila
M. pneumonia 
Streptococci (not staph)
Clostridium perfringens 
moraxella catarrhalis 
chlamydia spp
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60
Q

Azithromycin and clarithromycin have enhanced activity against?

A

MAC

mycobacterium Avium Complex

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61
Q

Resistance of macrolides

A

due to expression of the erm genes modifying the ribosomal traget and drecrease the affinity of the AB occurs. this is due to erm enzyme or methylase enzyme catalyse mono or demethylation of a specific adenine residue in the 23s rRNA. thus methyl group hinder the MLSb binding site

Efflux via
mrsA in staph
mefA in strep
mefe in s.pneumonia

62
Q

pk of erythromycin and distribution

A

the AB is inactivated by GI acid thus administrated with coated pellets that dissolve in duodenum.

food intake increase gi acid and decrease adsorption

Erythromycin ethly succinate is better in GI acid and less altered

all sites except brain and csf

63
Q

pk of clarithromycin

A

rapidly absorded from GIT, can be given with or without food

has a long half life due the active metabolite
14-hydroxyclarithromycin

64
Q

pk of azthromycin and distribution

A

rapidly absorded orally, should not be absorbed with food

all sites except brain and csf

high drug distribution thus prolonged t 1/2

65
Q

Comparative info of macrolides

A

Erythromycin is the natural drug and all the others have increase bioavialablility, higher peak conc, longer t1/2 and improved tissue conc

Azthromycin and clarithromycin have high uptake in granule zone of polymorphonuclear neutrophils

all are immunomodulatory and anti-inflammatory effects of macrolides are used in cystic fibrosis (azthromycin in lung function)

macrolides are not active against p.aeruginosa but resduce biofilm production & virulence factors

66
Q

Indications of macrolide drugs?

A

all are tx for Pc and Ceph allergy and pertussis

Azthromycin: chlamydial infections and CAP and MAC

Clarithromycin: better against MAC

no meningitis

67
Q

adverse effects of macrolides

A

E: GI SE

Only for C and E : increase in QT interval & cause torsade de ppointes

candidal infection
hypersensitivity
SJS
psychiatric distrubance

68
Q

Drug interactions for macrolides

A

atorvastatin:

clarithromycin will increase the conc of atorvastatin and risk of myopathy

69
Q

What are the tetracycline drugs? and broad or narrow spectrum? and bacteriostatic or bactericidal

A

Doxycycline
minocycline
tetracycline

broad spectrum

bactericidal at high conc but usually bacteriostatic

70
Q

MOA of tetracyclines

A

inhibit the protein systhesis by binding to the 30s subunit and blocking the tRNA (aminoacyl tRNA) from binding to the A site

71
Q

Spectrum for tetracycline

A

wide range of aerobic & anaerobic g+ve and g-ve (staph and strep)

72
Q

what drug is used to mo that is resistance to Tc?

A

Tigecycline

73
Q

Indications of tetracyclines

A

RTI (doxycycline –> CAP)

Skin and soft tissue infections -> MRSA

Acne (inihibition of propionibacteria)

intra-abdominal infections

STD (chlamydia trachomatis)

Minocycline: leprosy

74
Q

Pk of Tc

A

tetracycline poorly absorbed form GIT,
effected by food, di or trivalent cations, dairy product, antacids, Fe and Zn supplements

doxycycline and minocycline less affected by GI acid and orally absorbed

75
Q

Resistance of tetracyclines

A

efflux by tetK
ribosomal protection by tetM
Enzymatic inactivation of Tc

76
Q

Adverse effects of Tc

A

Tooth discolouration (in children , tetracycline calcium orthophosphate complex causes this)

reduced bone growth (calcification)

vestibular toxicity - minocycline

CDAD

77
Q

what are the glycopeptide drugs

A

Vancomycin and teicoplanin

78
Q

MOA of glycopeptides? bacteriostatic or bactericidal

A

Inhibit the call wall synthesis or elongation by binding to the 2 D-alanine residue of the free carboxy end of the pentapeptide. the binding sterically hinders the elongation of the peptidoglycan backbone.

bactericidal

79
Q

Spectrum for Glycopeptides

A

G +ve only (narrow)

MRSA
staph aureus
Strep (PPV)

80
Q

Resistance to glycopeptides

A

is a result of the alteration of d-alanyl-d-alanine to d-lactacte or d-serine.

Van A: d-lactate and both are resistant
Van B: teicoplanin as be used and d-lactate
Van C: non-transferable, constitutive, low level resistance to vancomycin and d-serine
Van D: non trasferable, resistance to vancomycin and reduced effect by teicoplanin, constitutive and d-lactate

Van E,G &L

81
Q

Pk of glycopeptides

A

both IV, vancomycin is widely distributed (csf) and teicoplanin as high plasma protein bound

82
Q

Indications for glycopeptides

A 
MRSA,
MRSE (multi resistant s. epidermidis)
Pc allergy 
CDAD 
prophylaxis in endocarditis in Pc hypersensitive
surgical prophylaxis in implantation
83
Q

Adverse Effects for glycopeptides

A

Red man syndrome
usually due to infusion being given too quickly. thus having a direct effect of vancomycin on the mast cells & basophihls. degraulation of mast cells cause release of histamine . Sx include fever, chills, itch, hypotension

management via slow infusion rate (>60 mins) and antihistamine (promethazine)

84
Q

Precautions for glycopeptides

A

allergy to vacomycin or teicoplanin
thrombocytopenia during Tx
Hearing impairment (increase of ototoxicity)
renal impairment (nephrotoxicity –> ototoxicity)

85
Q

What are the drug AB under aminoglycosides

A

Parenteral (Amikacin , Gentamicin , Streptomycin & Tobramycin)

Oral ( Neomycin )

Topical ( Framycetin)

86
Q

MOA of aminoglycosides and stages of uptake and how does it interfere with protein synthesis?

A

inhibits protein synthesis by binding irreversibly to the 30 s Subunit causing cell membrane damage –> cell death.

Diffuse throught eh porin in outer membrane of G-ve bacteria & enter the periplasmic space.
transported across cytoplasmic membrane via the oxygen dependent process. once inside the cytoplasm bings to the 30s Subunit irreversibly.

interferes with protein synthesis via:

  1. blocks the formation of the initiation complex
  2. blocks further translation of protein and produces premature protein
  3. incorporation of incorrect amino acid
87
Q

Resistance of aminoglycosides?

A

Antibiotic substituting enzyme , resistance is due to transferable plasmid mediated enzymes that modify the amino groups (N-acelytransferase) (AAC) and OH group (O-adenyltransferase (ANT) and O-phosphotransferase (APH)

88
Q

What drug is given if the strains are resistant to Aminoglycoside?

A

Amikacin

89
Q

Spectrum for Aminoglycoside? gentamicin activity?

A 
SPACE MP
Serratia 
Pseudomonas
Actineobacter
Citrobacter
Enterobacteriaceas
Morganella 
Providencia

Gentamicin is usedin hosptial acquired G-ve infections

90
Q

Adverse effects for aminoglycosides

A

Ototoxicity: caused by auditory and vestibular dysfunction due to the drug accumulation in the perilymph and endolymph. thus causing damage to sensory cells

Nephrotoxicity: Due to the accumulation and retention in the brush border cells of PCT. the drug alters the structure and function of the PCT cells causing decrease in excretion and thus leads to ototoxicity

Nueromuscular blockade

91
Q

Theory of once daily dosage for aminoglycosides

A
  1. Concentration Dependent Killing
  2. Concentration Dependent Post-Antibiotic Effect
  3. First Exposure Effect - Selection of resistant mutants less likely
  4. Less Nephrotoxicity - Renal accumulation & nephrotoxicity reduced
  5. Uptake into the Ear Reduced
  6. Efficacy Maintained
92
Q

Indications of aminoglycosides

A

Cystic fibrosis

93
Q

What are the lincosamide drugs?

A

clindamycin

lincomycin

94
Q

MOA of lincosamides?

A

inhibits protein synthesis by interfering with the formation of initiation complexes and translocation reactions

95
Q

Spectrum for Lincosamides

A 
G+ve (SSV)
- Strep pyogenes
- strep pneumonia 
-viridans strep
Anaerobic (BCF)
-bacteroides fragilis
-Clostridium difficle
-Fusobacteria spp

NO GRAM -ve

96
Q

Indications for lincosamides

A

Alternative in people with allergy to Pc and Cep

97
Q

Adverse effects for lincosamides

A

Clostridium difficile-associated disease
Mild to severe diarrhoea
o May have 5-20 watery bowel movements per day
• Malaise, anorexia, nausea
• Dehydration, fever (30-50% of patients)
• Abdominal pain & cramping
• Colitis, toxic megacolon
Treatment: Metronidazole 400mg tds for 10 days

98
Q

Drugs that are part of Streptogramins

A

Quinupristin 30% and dalfopristin 70%

99
Q

MOA of Streptogramins

A

Inhibit protein synthesis, binding to 50s Subunit

  • Dalfopristin interfers with polypeptide chain formation
  • Quinupristin inhibits elongation of proteins
100
Q

Indications for streptogramins

A

MRSA or VREF

101
Q

Adverse effect for sterptogramins

A

Infusion related events
CDAD
Hepatitis

102
Q

Linezolid MOA

A

Inhibits protein synthesis by binding to the p-site of the 50s Subunit and prevents the formation of initiation complex

103
Q

Spectrum for Linezolid

A

Aerobic and G +ve only

104
Q

Indications for linezolid

A

VRE and MRSA

serious g +ve infections

105
Q

Interesting about linezolid

A

linezolid is a weak reversible nonselective mono amine oxidase inhibitor. thus interaction with adrenergics causes hypertension and avoid foods rich with tyramine

when given with serotonergic drugs may cause serotonin syndrome => confusion and restlessness

106
Q

MOA of Chloramphenicol

A

Broad spectrum
inhibits the protein synthesis by binding to the 50s Subunit of the p-site thus preventing the transpeptidation reaction NOT THE TRANSLOCATION

107
Q

Spectrum of Chloramphenicol

A

gram +ve => staph aureus, strep

gram - ve => but no pseudomonas activity

108
Q

Indications for Chloramphenicol

A

Reserved for meningitis and others that resistant to other drugs

109
Q

Adverse effect for chloramphenicol

A

Grey baby syndrome:
sx such as refusal to suck, rapid respiration and loose green stools.
due to deficiency of glucuronyl transferase and inadequate renal excertion

110
Q

Resistance to chloramphenicol

A

Drug modifying enzyme (Ab substituting) -> chloramphenicol acetyl transferase

111
Q

Sodium fusidate MOA

A

Inhibits protein synthesis by preventing the translocation of the peptide subunit

112
Q

Spectrum for sodium fusidate

A

G +ve only —> Staph and MRSA

NO G -ve

113
Q

Indications for sodium fusidate

A

Staph infections –> osteomyelitis and burns

114
Q

Adverse effections for sodium fusidate

A

leucopenia

thrombocytopenia

115
Q

MOA of Mupirocin

A

AB conatin a structure similar to isoleucine. thus competes with isoleucine for binding to to isoleucine transfer RNA synthetase and prevent the formation of isoleucyl transfer RNA thus prevent the Isoleucine incoporation in proteins

116
Q

Spectrum for mupirocin

A

G +ve and selected g -ve strep and MRSA

117
Q

Indications for mupirocin

A

Mild impetigo
small skin lesions
nasal carriage of staph

118
Q

Lipopeptides drugs

A

Daptomycin

119
Q

MOA of daptomycin

A

Bactericidal activity by distrupting the plasma membrane without entering the cytoplasm. the acyl tail portion inserts into the plasma membrane in presence of Ca 2+ causing depolarisation of the membrane –> efflux of K+ ions (essential for DNA, RNA and protein synthesis) lead to cell death. leaves a ghost shell behind

120
Q

Indication of Daptomycin

A

Stap, MRSA

only G +ve

121
Q

Adverse effects and precautions

A

CDAD
multi-organ hypersensitivity syndrome

Myopathy is the precaution

122
Q

MOA of peptides

A

Acts like cationic detergents that interacts with phospholipids and disrupts the structure of the cell membrane

123
Q

Indications for peptides or polymyxins

A

G -ve only
Pseudomonas aeruginosa in cystic fibrosis

Gramicidin is a peptides that is active against gram +ve not g -ve and highly toxic to liver and kidneys

124
Q

Adverse effects for peptides

A

Nephrotoxicity and neurotoxicity

125
Q

MOA of Sulfonamides

A

Sulfonamides are structural analogues and competitive antagonists of para-aminobenzoic acid (PABA), this prevents bacterial utilisation of PABA for the synthesis of FOLIC acid. Sulfonamides have a higher affinity for the bacterial enzyme dihydropteroate synthase (DHPS) thus prevents PABA into incorporation into dihydropteroic acid.

126
Q

Drugs for sulfonamides?

A

Sulfamethoxazole is orally taken and Crystalluria is possible

Silver sulfadiazine is used to reduce microbial colonization and incidence of infections from burns

127
Q

MOA of trimethroprim

A

This Ab is a potent and selective competitve inhibitor of dihydrofolate reductase. this enzyme reduces dihydrofolic acid to tetrahydrofolic acid and inhibits the folate production

128
Q

Indication and contraindications for trimethroprim

A

Empirical treatment for uncomplicated lower UTI
Epididymo orchitis
Prostatitis

CI: Megaloblastic anaemia and hyperkalaemia

129
Q

Indications for sulfamethoxazole with trimethoprim

A

MRSA
Shigellosis
Melioidosis

130
Q

PK, adverse effects for sulfamethoxazole with trimethoprim

A

20:1 ratio (800 mg : 160 mg bd

Crystalluria and hyperkalaemia nad thromocytopenia

131
Q

Drugs for Quinolones

A

COMN

Ciprofloxacin
Ofloxacin
Moxifloxacin
Norfloxacin

132
Q

MOA for Quinolones

A

Inhibit bacterial DNA synthesis by blocking DNA gyrase (topoisomerase 2) and iopoisomerase 4. these 2 enzymes are involved in DNA synthesis and DNA replication.

Topoismerase 2 is involved in the replication, transcription and repair of bacterial DNA. In the DNA replication the double helical DNA is separated to all DNA polymerase to read. but separation results in supercoiling of the DNA in front of the point of separation. the DNA gyrase introduces negative supercoils to allow DNA synthesis to continue.

Quinolones ihibit nicking and closing of DNA gyrase activity

Topoismerase 4 is important in separating the daughter DNA copies during cell division

Quinolones block the decatenating activity of topoismerase 4

133
Q

Spectrum for 4 generation of quinolones

A

1st -> Modearte g -ve and minimal systemic distribution
2nd-> expanded g -ve activity and limited g+ve (ciprofloxacin & norfloxacin)
3rd -> expanded G -ve and improved G +ve converage
4th-> maintain G-ve and improved G+ve (moxifloxacin)

Ciprofloxacin for Pseudomonas aeruginomas

134
Q

Absorption, Distribution and Elimination of quinolones

A

Absorded well after oral administration. food doesn’t impair absorption but chelate with cations. dairy products, antacidsd, Fe and Zn supplement

Distribution t1/2 is 4-5 hrs and high volume of distribution

Elimination: most by kidney but moxifloxacin is by liver

135
Q

Indications for quinolones

A 
Ciprofloxacillin (PUSSPOET)
pertusis 
UTI
Salmonella 
shigellosis 
pseudonomas aeruginomas
otitis media 
epididmyo Orchitis 
Typoid 
Norfloxacillin (SPUD)
Shigellosis 
pseudomonas aeruginomas
UTI 
Diahorrea 
Moxifloxacillin (CCAST)
Chronic bronchitis
CAP
Anaerobic Bacteria 
Soft skin infections 
multi drug resistant TB
136
Q

Adverse effects in quinolones and precautions

A 
Tendon rupture
-Over 60 years
-Use of corticosteroid 
Organ transplant 
Renal impairment 
rheumatoid arthritis

Precautions: neurological (seizures) and cardiovascular

137
Q

MOA of fidaxomicin

A

inhibits bacterial transcription by binding to RNA polymerase, a large enzyme that consists of 5 subunits and fidaxomicin inhibits sigma subunit

138
Q

Spectrum, indications and adverse effects for fidaxomicin

A

Narrow spectrum. Activity against c.difficle, staphylococci and enterococci

Poorl absorded from GIT
Indicated for Clostridium Difficile infection
ADR : Hypersensitivity

139
Q

Nitrofurantoin MOA

A

by suspectible MO it is reduced to form a reactive intermediate that will inhibit enzyme that is required for DNA/RNA/Protein synthesis

140
Q

Spectrum and indications for Nitrofurantoin

and adverse effects

A

active against urinary pathogens
indicated for lower UTI

Drowsiness and allergic skin reactions

141
Q

MOA of Hexamine Hippurate

A

In kidney Hexamine hippurate dissociates to hippuric acid + hexamine
(methenamine)
◦ Methenamine is a urinary tract antiseptic & prodrug Is hydrolysed in acidic pH to ammonia & formaldehyde, which is bactericidal against G+ve & G-ve mo

142
Q

Indications and spectrum for Hexamine hippurate

A

Prophylaxis of chronic or recurrent lower UTIs

Active against G+ve & G-ve bacteria

143
Q

Pk for hexamine hippurate

A

Readily absorbed orally
Mainly excreted unchanged in the urine
The decomposition reaction is fairly slow
Methenamine is distributed throughout body fluids but no decomposition of the drug occurs at pH 7.4 ∴ systemic toxicity should
not occur

144
Q

CI for hexamine hippurate

A

Severe dehydration
Gout
Hepatic insufficiency

145
Q

drugs under nitroimidazoles

A

Metronidazole

Tinidazole

146
Q

MOA of nitroimidazoles

A

Both drugs are prodrugs, removes electrons from ferredoxin (ferredoxins donate electron -> highly reactive nitro radical is produced and this damages DNA) causing the nitro group of the drug to be reduced. the reduced intermediate is highly reactive and binds to DNA which undergoes Strand breakage

147
Q

Spectrum for nitroimidazoles

A

Anaerobic (BCF)

Protozoa (Trichomonas vaginalis and gradnerella vaginalis)

148
Q

resistance for nitroimidazoles

A

Metabolic changes and increased O2 levels results in poor penetration and reduced activity

149
Q

Indication for nitroimidazoles

A

CDAD
bacterial vaginosis
Tinidazole (protozoal infection)

150
Q

Adverse effects for nitroimidazoles

A 
furry tongue 
slossitis 
stomatitis 
SJS
Headache

AC (1 decks)

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