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Pharmacology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Mechanism of action of penecillin

A

Interferes with last step of bacterial cell wall synthses: cross linkage via acting on transpeptidase enz

Acts on PBS(cell memb proteins :synthsis and maintaince of cell wall) out of which transpeptidase is one

Continuous action of autolysin(degradative enz for cell wall remodelling) even in the abscens of cell wall synthsis

Results in osmotically less stable memb

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2
Q

Cephalosporin moa

A

Same as penecillin

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3
Q

Doc for gas gangrene/C.perforinges

A

Penecillin

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4
Q

Doc for syphilis

A

Penecillin

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5
Q

Diff penecillin V and G

A

G: parenteral

V: more stable so orally

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6
Q

All B lactams are excreted via urine except

A

Nafcillin

Oxacillin

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7
Q

Penecillin G used for

A

Gp and GN cocci
GP baciili
Spirichets

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8
Q

Adverse effect of methicillin

A

Intersitial nephritis,Hematuria,albuminuria

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9
Q

Extended spectrum penecillins work against

A

Same as penecillinG but more for GNB

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10
Q

Classification of penecillins

A

PenecillinV/G

B lactamase resistant:methicillin etc

Extended spectrum:amoxi, ampi,piperacillin
etc

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11
Q

Doc for listeria

A

Ampicillin

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12
Q

Egs of antipseudomonal penecillins

A

Ticarcillin

Piperacillin

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13
Q

piper/ticarcillin ___ to pencillase producing organism

A

Senisitive

So given along with tazobactam and clavulinic acid respectively

Tt not together

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14
Q

piper/ticarcillin ___ to pencillase producing organism

A

Senisitive

So given along with tazobactam and clavulinic acid respectively

Tt not together

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15
Q

Extended spectrum penicillins are _____ to B lactamase producing org

A

Sensitive

Amoxi clavulinic acid

Ampi-sulbactum

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16
Q

Depot forms of penecillins

A

Absorbed slowly into circulation and persist at low levels over a long period

Given IM

Eg: procaine Penicillin G, benzathine P G

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17
Q

Method of Excretion of penicillins from kidney

A

.Organic acid (tubular) secretory system

.filteration

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18
Q

Effect of probenecid on penicillin level

A

Increase P levels

Competes for active tubular secretion via organic acid transporter so inhibits P secretion.

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19
Q

Route of penecillin G

A

Iv, Im

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20
Q

Can penecillin penetrate CNS

A

Until they are inflamed (inflammation disrupts BBB leading to increased permeability)

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21
Q

Spectrum of cephalosporins with respect to staph

A

All generations scan work against MSSA not MRSA

EXCEPT newer 5th generation cephalosporin: ceftaroline

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22
Q

5th generatiom cephalosporin

A

Ceftaroline

I.v.

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23
Q

No B lactam is effective against MRSA except__

A

5 th generation cephalosporin

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24
Q

All cephalosprins are excreted via urine except

A

Ceftriaxone

Cefoperazone (both 3 rd gen)

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25
Q

Which cephalosprins penetrate BBB

A

All 3 rd gen : except cefoperazone

Only one of 2 nd gen : cefuroxime

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26
Q

Ist generation cephalosprins drugs

A

Dro-zo-le
Cepha/cefa except cefaclor (2 nd gen)

Cefadroxil
Cephazolin
Cephalexin

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27
Q

Cephalosprins spectrum

A

1 gen : GP high , GN weak (like penecillin G)

2 gen :GN high ,GP and anaerobes weak

3gen: GN high + few pseudo , GP and anaerobes weak

4th gen:same as 3 rd

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28
Q

Why is cilastatin combined with imipenem

A

To protect it from metabolism by renal dehyropeptidase (brush border of proximal tubule) which converts into a NEPHROTOXIC metabolite

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29
Q

Most cephalosporins do not penetrate CSF except

A

Third gen cephalosporins

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30
Q

Carbapenems spectrum

A

GP (B lactamase producing)
GN
Anaerobes
PSEUDOMONAS

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31
Q

Peculiar side effect of imepenem

A

Seizures

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32
Q

3 rd gen cephalosporin active against pseudomonas

A

Ceftazidime

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33
Q

Monobactam spectrum

A

Aerobic GNB only
(Not against GP and anaerobes)
Same as aminoglycosides

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34
Q

______ may offer a safe alternative for treating patients who are allergic to pencillins, cephalosprins, carbepenems

A

AZTREONAM because of less cross reactivity

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35
Q

B lactams

A

Penicillins
Cephalosporins
Monobactams
Carbepenems

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36
Q

Vancomycin use

A

(Maily GP)
MRSA

C.difficile( 2nd choice to metronidazole)

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37
Q

Moa of vancomycin

A

Prevents release of peptidoglycan units release from carrier

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38
Q

Red man syndrome seen with

A

Vancomycin
Infusion related
Due to release of histamine

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39
Q

Daptomycin moa

A

Act on cell membrane

Produces membrame channel and membrane leakage

This causes rapiddepolarization, resulting in a loss of membrane potential leading to inhibition ofprotein,DNA, andRNAsynthesis, which results in bacterial cell death.

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40
Q

Daptomycin use

A

GP(including MRSA) for complicated skin infections and bacterimia

Cannot be used in Rx of pneumonia because inactivated by surfactant

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41
Q

vancomycin
Daptomycin
Telavancin
Spectrum?

A

GP
MRSA
Strepto(including penecillin resistant)
Enterococci (including susceptible to vancomycin)

All IV except vanco i.e. oral too

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42
Q

Televancin moa

A

Inhibitss both bacterial cell wall synthseis

and cell memb

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43
Q

SE of vancomycin

A

Red man syndrome

Oto and nephrotoxic

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44
Q

Fosfomycin moa

A

Inhibits a transferase enz which catalyses first step in peptidogylcan sythesis
(P last step- transpeptidase- cross linking)

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45
Q

Fosfomycin use

A

UTI caused by E.coli/faecalis/ fecium

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46
Q

Polymxins moa

A

GN

Binds to phospholipids of GN cell membrane

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47
Q

Use of polymxins

A

For GN bacteria

Includes
1.Polymxin B- PE, oph,otic, topical

2.Colistin/polymxin E- I.V , inhaled

Se: nephro and neurotoxicity when given systemically

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48
Q

Moa of tetracylines

A

Inhibit protien synthesis by binding to 30S ribosome & inh. aminoacyl tRNA attachment to ‘A’ site

Static

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49
Q

Tetracyline spectrum

A

Broad s -GN & GP

Highly R-entero, myco, pseudo

Highly S-spiroch, rickettsia, chlamydia

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50
Q

Absorption of tetracylines

A

Administration with dairy products or other substances that contain divalent and trivalent cations (for example, magnesium and aluminum antacids or iron supplements) decreases absorption, particularly for tetracycline , due to the formation of nonabsorbable chelates

Tetracyline drug should be taken empty stomach rest are absorbed irrespective of food (but take care of above point)

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51
Q

Ecxretion of tetracyclines

A

Urine except doxycyline(bile)

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52
Q

______ are theTetracylines achirving therapeutic comcentration in CSF

A

Doxy

Mino

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53
Q

Drugs causing phototoxicity

A

Tetracylines
Sulfonamides
FQs

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54
Q

Drug causing pseudotumor cerebrii

A

Tetracylines

Benign, intracranial hypertension characterized by headache and blurred vision may occur rarely in adults.

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55
Q

Side effects of tetracylines

A

Gastric discomfort , esophagitis- mucosal irritation

Effects on calcified tissues-
Teeth :Brown dis, ill formed, prone to caries.
Bone:deformity and reduction in height
(Child and pregnancy)

Hepatotoxicity

Phototoxicity

Ototoxic

Pseudotumor cerebrii

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56
Q

Tigecycline

A

Act ag bac. that had dev resist to ttc

Also broad S

Not active ag. Pseudo and proteus

Active ag. Enterobacteriacae

Moa- same

Lack of cross resist. Bw ttc and it

Route- i.v

Ex: bile mainly

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57
Q

Contraindications of teyracycline

A

Children and pregnancy

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58
Q

Ototoxic antimicrobials drugs

A

vancomycin
Tetracycline
Aminogycoside
Macrolide

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59
Q

Concurrent administration of AG with neuromuscular blockade should be avoided.
why?

A

interfere with calcium ions movements through the calcium channels of the membrane of the motor nerve-endings inhibiting acetylcholine release at the synaptic cleft.

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60
Q

AGs moa

A

Binds to 30S subunit, distorting its structure and causing misreading of the mRNA

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61
Q

Antibiotics that disrupt protein synthesis are generally ___ however, aminoglycosides are unique in that they are _____

A

Bacteriostatic

Bacterocidal

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62
Q

extended interval dosing (a single large dose given once daily) is now more commonly utilized than divided daily doses in case of AGs .Why?

A

The bactericidal effect of aminoglycosides is concentration dependent; that is, efficacy is dependent on the maximum concentration (Cmax) of drug above the minimum inhibitory concentration (MIC) of the organism.

The larger the dose, the longer the PAE
PAE (post Ab effect) is continued bacterial suppression after drug levels fall below the MIC.

reduces the risk of nephrotoxicity and ototoxicity

increases convenience.

63
Q

AGs spectrum

A

Aerobic GN bacilli including pseudomonas

64
Q

Route of administration of AGs

A

Parentral-i.v , i.m. itrathecal

The highly polar, polycationic structure of the aminoglycosides prevents adequate absorption after oral administration.(except neomycin)

65
Q

AGs does/ not penetrate CSF

A

Does not
Even when inflamed
So intrathecal

66
Q

SE of AGs

A

Ototoxicity
Nephrotoxicity
Neuromuscular blockade
Allergic

67
Q

AGs excretion

A

All via urine

68
Q

Neomycin

A

Against GNB

Topical: skin infn

Oral:Prep of bowel before surgery to reduce PO infn
Hepatic coma-dec NH3by inh bacterial flora(lactulose)

69
Q

Neomycin

A

Against GNB

Topical: skin infn

Oral:Prep of bowel before surgery to reduce PO infn
Hepatic coma-dec NH3by inh bacterial flora(lactulose)

70
Q

Triple ointment

A

Neomycin+polymyxin+bacitracin

Out of the above neo cause contact dermatitis

Polymixin,neomycin=GN
Bacitracin=GP

71
Q

Moa of macrolides

A

Bind to 50S rib, prevent translocation of peptide chain from A to P site

72
Q

csf penetration of macrolides

A

Does not penetrate

73
Q

_____macrolides is eff against many of the same org as penicillin G

A

Erthryomycin

74
Q

RX of M.pneumonae

A

Azithromycin or doxycyline

75
Q

Rx of chlamydia

A

Azithromycin or doxyxline

76
Q

Macrolide used in MAC

A

Azithromycin

77
Q

Rx of MAC

A

Erthyromycin , rifampin , ethambutol

78
Q

spectrum of macrolides

A 
Gpc (not MRSA)
Clamydia
Mycoplasma
Mycobacteria
Spirochete
h.pylori
C. Jejuni
Legionella
H.influenza
79
Q

Excretion of macrolide

A

All bile (azith/eryth/telithro) except clarthromycin , urine

80
Q

Se of macrolide

A

.Git-epigastric pain

+motilin R -promotes int motility without affecting colon

Used in diabetic gastroparesis and postop ileus

But tolerance develops and flora eff :not used as prokinetic

Ototoxic:high dose

Hypersenstivity

Hepatitis:estolate

81
Q

Drug interaction of macrolide with CYP450

A

.All are enz inhibitors(cla/erythro/telith) except AZITHROMYCIN

82
Q

Moa of macrolide

A

.Bind to 50S rib, prevent translocation of peptide chain from A to P site

83
Q

Fidaxamycin moa, spectrum and use

A

Similar to macrolide

Binds RNA polymerase and inhibits transcription

GP aerobe and anaerobe only

C.difficile(minimal systemic abspn)

84
Q

Chloramphenicol moa

A

chloamp

50s-inh peptidyl transferase

*macrolides & clinda:

50s-prevents translocatn from a to p site

85
Q

50S ribosomal subunit is the target of

A

Macrolides,Clindamycin

Chloramphenicol

Quinupristin/dalfopristin

Linezolid

86
Q

Excretion of chloamphenicol

A

Metabolised by liver via glucuronidation and in urine

Dose reductions are necessary in patients with liver dysfunction or cirrhosis.

87
Q

CSF penetration of chloramphenicol

A

Yes

“Phen”-lipid solubility

88
Q

SE of chloramphenicol

A

ANEMIA

  • hemolytic anemia(in G6PD def)
  • aplastic (BM suppression Due to some similarity of mammalian mitochondrial ribosomes to those of bacteria)

GRAY BABY

ENZ INHIBITOR

89
Q

Grey baby syn caused by

A

CHLORAMPHENICOL

Neonates have a low capacity to glucuronidate the antibiotic, and they have underdeveloped renal function. Therefore, neonates have a decreased ability to excrete the drug, which accumulates to levels that interfere with the function of mitochondrial ribosomes. This leads to poor feeding, depressed breathing, cardiovascular collapse, cyanosis (hence the term “gray baby”), and death.

90
Q

Chloramphenicol spectrum

A

GP and GN (Broad like teyracycline and macrolides)

91
Q

GP and GN

A 
Chloramphenicol
Tetracycline
Macrolides
Sulfonamides
Carbepenems
92
Q

Clindamycin spectrum

A

GP (including MRSA, strepto, ANAEROBES)

93
Q

Clindamycin adr

A

Pseudomembranous colitis by C.difficile

94
Q

Quinupristin/dalfopristin

A

Mixture

Moa- binds to separate sites on 50S

Use: E.faecium including VRE vamcomycin resistant enteroccoci

95
Q

Linezolid spectrum

A

GP mainly

VRSA and VRE

96
Q

Linezolid moa

A

Binds to P site of 50S rib and distorts tRNA binding site -inh formn of initiation complex

97
Q

Linezolid adr

A

Bm depression , thrombocytopenia

N, v, headache,git upset , rash

Optic neuritis , peripheral neuropathy (>28days)

Not to be given with MAO inh, SSRI,dietry tyramine.( nonselective monoamine oxidase inhibitor activity and may lead to serotonin syndrome)

98
Q

MRSA antibiotics

A 
ORAL
TMP-SMX
Doxy,minocyline
Clindamycin
Linezolid
IV
Vancomycin
Linezolid
Clindamycin
Daptomycin
Telavancin
99
Q

Moa of FQs

A

Cidal

INHIBITS TOPOISOMERASE II/DNA GYRASE
relieves strain while double stranded DNAis being unwound byhelicase.The enzyme causes negativesupercoilingof the DNA or relaxes positive supercoils.

TOPOISOMERASE IV
First, it is responsible for unlinking, or decatenating, DNA followingDNA replication. The double-helical nature ofDNAand itssemiconservativemode of replication causes the two newly replicated DNA strands to be interlinked. These links must be removed in order for thechromosome(andplasmids) to segregate into daughter cells so that cell division can complete.

Topoisomerase IV’s second function in the cell is to relax positivesupercoils. It shares this role with DNA gyrase, which is also able to relax positive supercoils. Together, gyrase and topoisomerase IV remove the positive supercoils that accumulate ahead of a translocatingDNA polymerase, allowingDNA replicationto continue unhindered by topological strain.

100
Q

Respiratory FQs

A

Levofloxacin and moxifloxacin

101
Q

FQs spectrum

A

4 generations

GN mainly but As the gen increase more action against GP

1-naldixic acid
2- GN and atypical :norfloxacin , cipro
3- inc GP,GN: levofloxacin
4-GP and anaerobic: moxifloxacin

102
Q

FQs which is highly efficacious in dirrhoeal diseases

A

Ciprofloxacin

103
Q

FQ with Anaerobic activity

A

Moxifloxacin

104
Q

FQ used for UTIs

A

Ciprofloxacin

Levofloxacin

105
Q

Uses of FQs

A 
Respiratory-levo, moxi
Git infections-cipro
Anthrax-cipro
UTIs-cipro , levo
Anaerobic - moxi
Cystic fibrosis for psedomonas- cipro
Typhoid- cipro
TB
Prostitis
106
Q

Excretion of FQs

A

Via urine except MOXIFLOXACIN which is excreted primarily by liver

107
Q

Csf penetration of FQs

A

No

108
Q

Absorption of FQs

A

Ingestion of fluoroquinolones with sucralfate,

aluminum- or magnesium- containing antacids,

dietary supplements containing iron or zinc

Calcium and other divalent cations also interfere with the absorption of these agents

109
Q

FQs adr

A

N/c/d

Headache, dizziness,lightheadedess ( caution in CNS disorder)

Phototoxicity

Arthropathy/ articular cartilage erosion in animals

Tendinitis/tendin rupture

QT prolongation - moxifloxacin

Drug interaction?

110
Q

Sulfonamides spectrum

A

Bacteriostatic

GN+GP

Not anaerobic

111
Q

Sulfonamides moa

A

Structural analogue of PABA, inh de novo folate synthsis in bacteria , so folic acid is not formed

112
Q

What is cotrimoxazole

A

Sulfmethoxazole (sulfonamide) + pyimethamine

The sulfonamides (sulfa drugs) are a family of antibiotics that inhibit de novo synthesis of folate : PABA analogue and inhibits dihydo pteroate synthase.

A second type of folate antagonist—trimethoprim—prevents microorganisms from converting dihydrofolic acid to tetrahydrofolic acid, with minimal effect on the ability of human cells to make this conversion by inhibiting dihydrofolate reductase.

113
Q

Sulfonamide for toxoplasmosis

A

Sulfadiazine + pyrimethamine

114
Q

sulfasalazine use

A

Not absorbed after oral administration

INFLAMMATORY BOWEL DS

Local intestinal flora split sulfasalazine into sulfapyridine and 5-aminosalicylate, with the latter exerting the anti-inflammatory effect. Absorption of sulfapyridine can lead to toxicity in patients who are slow acetylators.

115
Q

Silver sulfadiazine

A

Topical

Burns to prevent colonisation

Silver sulfadiazine is preferred because mafenide produces pain on application and its absorption may contribute to acid–base disturbances.

116
Q

What is Significance of sulfonamides being highly bound to albumin?

A

KERNICTERUS- displace bilirubin from albumin , inc free bilirubin which can pass through immature BBB

WARFARIN:Transient potentiation of the anticoagulant effect

METHOTREXATE: inc

117
Q

Drug interactions of FQs

A

Only Ciprofloxacin inhibits CYP450

Inc theophylline , warfarin , cyclosporine

118
Q

CSF penetration of sulfonamides

A

Yes

119
Q

Excretion of sulfonamides

A

Unchanged drug + acetylated metabolite( acetylation done by LIVER) appear in urine

120
Q

Sulfonamides adr

A

CRYSTALLURIA- by acetylated metabolite

HYPERSENITIVITY- rash , angioedema , SJS

HEMATOPOITIC DISTURBANCE- hemolysis in G6PD def. , granulocytopenia , thrombocytopenia.

KERNICTERUS

DRUG POTENTIATION of the ones bound to albumin

121
Q

CI of sulfonamide

A

Allergy

Newborns and infants

Pregnant women at term(due to kernicterus)

122
Q

Trimethoprim moa

A

Prevents formation of tetrahydrofolic acid from dihydrofoloc acid by inhibiting dihydrofolate reductase

123
Q

Why trimethoprim does not effect mammilian enzymes

A

. The bacterial reductase has a much stronger affinity for trimethoprim than does the mammalian enzyme, which accounts for the selective toxicity of the drug.

124
Q

Trimethoprim spectrum

A

Similar to sulfonamides

125
Q

Trimethoprim adr

A

Folic acid deficiency especially in preg and those having poor diet

126
Q

Why trimoprim amd sulfamethoxazole are combined

A

Synergistic activity by inhibition of 2 sequential steps in the formation of folic acid.

Same half life

Both can cross CSF

Spectrum becomes broader

Both distribute throughout the body and can cross BBB

127
Q

Antibacterial spectrum of cotrimoxazole

A

respiratory tract infections- Pneumocystis jerovicii, H .influenza, Legionella

Toxoplasmosos

Git infections-shigellosis , nontyphoid salmonella,Salmonella carriers

MRSA

Nocardia

Cross BBB

Listeria(ampicillin)

UTI and Prostatic inf ( trimethoprim concentrates in prostatic and vaginal fluid)

128
Q

Excretion of cotimoxazole

A

Parent drugs and metabolites excreted in urine

129
Q

Csf penetration of cotrimoxazole

A

Yes by both the components

130
Q

Adr of cotrimoxazole

A

Git -n ,v

Skin rash

Hematologic - anemia , leucopenia , thrombocytopenia(REVERSED BY CONCURENT ADMINISTRATION OF FOLINIC ACID: protects patient but does not enter org because they are impermeable to it)

Hemolytic anemia in G6PD def- sulfamethoxazole

Displacement of albumin bound drugs’ sulfamethoxazole

131
Q

UTIs drugs used

A

Cotrimoxazole

FQs

132
Q

Methenamine moa

A

Methenamine decomposes at an acidic pH of 5.5 or less in the urine, thus producing formaldehyde, which acts locally and is toxic to most bacteria .

Methenamine is frequently formulated with a weak acid (for example, mandelic acid or hippuric acid) to keep the urine acidic.

The urinary pH should be maintained below 6. Antacids, such as sodium bicarbonate, should be avoided.

133
Q

Methenamine use

A

Lower UTI

Not upper UTI(eg: pyleonephritis) because of alkalinzation of urine by urea splitting org eg: proteus

134
Q

Why methenamine is CI on hepatic inficiency and renal insufficiency?

A

Methenamine is broken down into formaldehyde and NH3 in bladder .

NH3 has to be converted into urea by liver but in hepatic insufficiency NH3 accumulates.

Methenamine mandelate is contraindicated in patients with renal insufficiency, because mandelic acid may precipitate.

135
Q

Why sytemic toxicity of methenamine does not occur

A

No decompostion of the drug to its active metabolite occur in ph 7.4

136
Q

Methenamine adr

A

Git

Higher doses: albuminuria, hematuria

137
Q

Why sufonamodes and methenamine should not be given concurrently

A
  1. S react with formaldehyde and mitual antagonism

2. Inc crystalluria

138
Q

Abs which do not penetrate at all

A

Macrolides
FQs
Aminoglycosides

139
Q

Enz inhibitors

A

Ciprofloxacin only
All amcrolides except azithromycin
Chloramphenicol

140
Q

Antibiotics whose absorption is effected by cations in food

A

FQs

Tetracylines

141
Q

Spectrum of

  1. Vancomycin
  2. Daptomycin
  3. Telavancin
A 
COMMON:GP
Staph aureus( MRSA)
Stepto.pyogenes , agalactiae
Strepto.pneum (penecillin resistant)
E.fecalis, fecium (vacomycin susceptible)

UNIQUE
1.C.difficile

  1. VRE(gecium/ fecalis)
  2. some VRE
142
Q

Fosfomycin

Fadaxamycin

A

UTI

C.difficile

143
Q

Lincosamides

A

Clindamycin drugs

144
Q

Pseudotumor cerebrii

A

Isotretinoin

Tetracylines

145
Q

Doc for legionella infection

A

Macrolides (especially azithromycin)
&
Respiratory floroquinolones

146
Q

Doc for H.influenzae

A

Cephalosporins( eg: ceftriaxone , cefotaxime)

147
Q

Doc for gonococcal infection involving cervix , urethra , pharynx , rectum

A

Ceftriaxone IM single dose + (Rx for Chlamydia if its infection is not ruled out) azithromycin PO OR doxycycline PO

148
Q

Doc for meningoccocal infections

A

Third gen cephalosporins

149
Q

Doc for pertussis

A

Macrolides

150
Q

Doc for gas gangrene

A

Penecillin + clindamycin

151
Q

Doc for tetanus

A

Metronidazole or penecillin

Not used in botulism

152
Q

Doc for listeria

A

Ampicillin

153
Q

Doc for diphtheria

A

IM PenecillinG then oral penecillin V
Or
Erythromycin

Pharmacology (16 decks)

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