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Pharmacology > Protein Synthesis Inhibitors II > Flashcards

Protein Synthesis Inhibitors II Flashcards

1
Q

Name the tetracyclines

A

TDM
Tetracycline
Doxycycline
Minocycline
Lymecycline
Oxytetracyline

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2
Q

What are Tetracycilnes

A

are crystalline Amphoteric molecules with low solubility: have an acidic and basic functional group–> not soluble

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3
Q

Name the a new drug class derived from Minocycline

A

Glycylcyclines

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4
Q

Name a Glycylcycline

A

Tigecycline: IV

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5
Q

Use of Tigecycline

A

treatment of resistant infections where tetracyclines on their own aren’t enough
Complicated skin, soft tissue, intr-abdominal infections

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6
Q

Uses of Tetracycline

A

Combination with other agents for treatment of Malaria
DOC in: Rickettsia
Chlamydia
Brucellosis
Mycoplasma infections
Spirochetal infections
Acne: due to its good skin penetrability
Chronic Bronchitis

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7
Q

Doxycyline uses

A

Prophylaxis of malaria

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8
Q

MOA of Tetracyclines

A

Bind to 30S subunit–> prevents formation of initiation complex=inhibits codon-anticodon interactions

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9
Q

How do the Tetracyclines enter the cell

A

move into micro-organisms via passive diffusion through the porins and energy dependent process of active transport

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10
Q

Resistance mechanisms against Tetracyclines

A
  1. Decr. intracellular accumulation as a result of decr. influx or active efflux (production of active Efflux pump that pumps the Tetracyclines out of the cell)
  2. Production of protein that interferes with the binding of Tetracyclines on Ribosome
  3. Enzymatic inactivation of drug
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11
Q

Admin of Tetracyclines

A

Orally with variable absorption
*taken with adequate amount of fluid
*Avoid antacids or milk as it prevents their absorption

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12
Q

Why is adequate fluid intake needed with Tetracyclines

A

to prevent drug capsules from sticking to bottom of Esophagus on mucosal lining=ulceration and pain
*need to remain upright for at least 30mins to prevent occurrence of Ulceration

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13
Q

PK benefits of newer Tetracyclines

A

Doxycycline and Minocycline
1. more lipid soluble–> near complete absorption in the presence of food
2. less incline to chelate

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14
Q

How do Antacids prevent the absorption of Tetracyclines

A

They contain Multivalet cations that form insoluble complexes with the Tetracyclins

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15
Q

Distribution of Tetracyclines

A

widely distributed
*cross placenta and excreted in breast milk

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16
Q

Excretion of newer Tetracyclines

A

mainly in bile thus its safer for renally impaired people

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17
Q

SEs of Tetracylcines

A

Cause GIT disruptions: dose-related NV
2. Destruction of normal gut flora=superinfections with Candida
3. Pseudomembranous Colitis: C.difficile can occure
4. Elderly patients: hepatotoxic effects
5. Photsensitivity
6. Deposited in bone and teeth: esp. young children
7. Causes bone growth retardation in children
8. Discolouration of nails+teeth and occasion Enamel Hypoplasia in kids
9. Potentially nephrotoxic effects
10. Reduced efficacy of COC

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18
Q

SEs of Minocycline

A

Blue-grey pigmentation of skin and pigmentation of acne scars
Vestibular toxicity

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19
Q

SEs of Tiglecycline

A

Incr. mortality and treatment failure seen

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20
Q

DIs with Tetracyclines

A
  1. CYP450 induces like Carbamazepine, phenytoin, barbiturates
  2. Vit A and other Retinoids: enhanced risk of incr. intracranial Pressure
  3. COC
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21
Q

Cautions of Tetracylcines

A

SLE: Minocycline
Myasthenia Graves: have weak neuromuscular blocking effects
Hepatic impairment
Porphyria
Elderly

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22
Q

CIs of Tetracyclines

A

Pregnancy
Children <8-12 yrs`

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23
Q

What is Chloramphenicol

A

Broad spectrum Bacteriostatic antibiotic

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24
Q

When is Chloramphenicol used as 1st line drug

A

rarely because of its potential toxicity: depresses bone marrow

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25
Q

Chloramphenicol is reserved for

A

severe infections by susceptible organisms due to potential to cause aplastic anemia

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26
Q

Spectrum/Uses of Chloramphenicol

A

Rickettsial infections: standard drugs CIed
Bacterial meningits: standard drugs CIed
Typhoid fever
Bacterial eye infections: topical

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27
Q

Chloramphenicol is active against

A

Chlamydia
Mycoplasma infections
Streptococci
Staphylococci
Hemophilus infections
Anaerobes

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28
Q

MOA of Chloramphenicol

A

powerful inhibitor of Protein Synthesis
Attaches reversibly to 50S subunit–> interferes with MOA of Peptidyl transferases

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29
Q

MOA of Peptidyltransferase

A

catalyses formation of peptide bind btwn growing peptide and new AA
=peptide cant grow further

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30
Q

Resistance mechanism against Chloramphenicol

A

Production of Chloramphenicol Acetyltransferase that inactivates the drug

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31
Q

Admin of Chloramphenicol

A

Chloramphenicol succinate: parenteral
–> highly water soluble where it gets hydrolysed to free Chloramphenicol

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32
Q

Distribution of Chloramphenicol

A

widely distributed
*high levels in brain and CSF: effective against meningitis

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33
Q

Metabolism of Chloramphenicol

A

in liver and after Glucuronide formation its excreted in urine

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34
Q

SEs of Chloramphenicol

A
  1. Serious IRREVERSIBLE Bone Marrow Depression–> idiosyncratic–> fatal aplastic anemia (esp. topical use)
  2. Dose-related reversible Bone Marrow Toxicity
  3. Reduced Efficacy of COC
  4. Use with great care in babies as ineffective conjugation with Glucuronic acid and excretion of drug cause: GREY BABY SYNDROME
  5. GIT effects
  6. Optic or peripheral neuritis
  7. Hypersensitivity rxns and jaundice
  8. Inhibits liver enzymes
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35
Q

GREY BABY SYNDROME is characterised by

A

abdominal distention
cyanosis
vasomotor collapse
Failure to feed

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36
Q

DIs with Chloramphenicol

A
  1. Causes CYP450 Inhibition: incr. conc. of Phenytoin, warfarin, sulfonylureases
  2. CYP450 inducers: decr. efficacy of Chloramphenicol
  3. Vit B, folic acid and iron: Chloramphenicol may interfere with Hematological response
  4. COC
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37
Q

Cautions in Chloramphenicol

A

Impaired hepatic function
Bone marrow depression: cancer, HIV patients

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38
Q

CIs of Chloramphenicol

A

Allergy
Porphyria
3rd trimester of pregnancy
Neonates
Lactation

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39
Q

Spectrum/Uses of Clindamycin

A

Susceptible gram +ive infections in patients allergic to Penicillins
Susceptible Staphylococcal and Anaerobic infections
Severe soft tissue infections
Lung Abscesses
Quinsy: not responding to Penicillins

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40
Q

Clindamycin is inactive against

A

Enterococci

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41
Q

MOA of Clindamycin

A

Inhibits protein synthesis by:
binds to 50S subunit–> interferes with formation of initiation complex–> inhibits translocations

42
Q

Different dosages of Clindamycin cause

A

Low: Bacteriostatic
High: Bactericidal

43
Q

Resistance mechanisms against Clindamycin

A

Mutation of ribosomal binding site
enzymatic inactivation

44
Q

Admin of Clindamycin

A

Oral, IV, IM
*taken with adequate fluid to prevent ulceration

45
Q

Metabolism and Excretion of Clindamycin

A

M; liver
E: mainly in bile, small unaltered amount in urine

46
Q

Distribution of Clindamycin

A

widely distributed
*doesn’t enter CSF

47
Q

SEs of Clindamycin

A

ND: oral, IV,IM
skin rxns
Transient incr. in liver enzymes+bilirubin
Transient Leucopenia, Thrombocytopenia, Agranulocytosis, Eosinophilia
Pseudomembranous Colitis: potentially fatal complication
Reduced efficacy of COC

48
Q

DIs with Clindamycin

A

COC

49
Q

Caution in Clindamycin

A

GIT disease
severe hepatic impairment
porphyria
elderly
pregnancy/lactation

50
Q

What is Fusidic Acid

A

Steroid antibiotic thats usually given Orally/Topically

51
Q

Spectrum/Uses of Fusidic Acid

A

Severe Staphylococcal infections
Combine with Cloxacillin (antistaphylococcal) to prevent emergence of resistance
Topically: acute skin infections (5days) and conjunctivis

52
Q

SEs of Fusidic Acid

A

Reversible Hepatotoxicty
GIT effects: take with meals
Kernicterus risk in Neonates
AVoid in Pregnancy
IM: local tissue necrosis
Local Hypersensitivity rxns

53
Q

DIs of Fusidic acid

A

Hydrocortisone: decr. Antibiotic activity and reduced efficacy of Fusidic acid
Statins: incr. risk of Rhabdomyolysis

54
Q

CIs of Fusidic Acid

A

Hepatic Dysfunction: as its excretd in bile

55
Q

Spectrum of Mupirocin

A

Gram +ive ONLY
Effective against Methicillin-resistant Stapylococcal aureus (MRSA)

56
Q

MOA of Mupirocin

A

Reversibly binds to Isoleusine-tRNA Synthetase and prevents formation of Isoleusine-tRNA
–>inhibits protein and RNA synthesis

57
Q

High dosages of Mupirocin results

A

in Bactericidal effects

58
Q

Admin of Mupirocin

A

Topical only + intranasal
*rapidly inactivated after absorption if given orally

59
Q

SEs of Mupirocin

A

Mild stinging
Burning
Itching at site of application

60
Q

Caution in Mupirocin

A

Porphyria

61
Q

What are Ketolides

A

Semi-synthetic deruvatives of Erythromycin A–> have broader Spectrum

62
Q

Name a Ketolide

A

Telithromycin

63
Q

Spectrum/Uses of Ketolides

A

similar spectrum to macrolides, H.influenzae
Erythromycin-resistant strains of Pneumoccoccus

64
Q

MOA of ketolides

A

Can bind to 2 sites on bacterial ribosome with higher affinity than macrolides
*may inhibit formation of newly forming Ribosomes

65
Q

SEs of Ketolides

A

Inhibit Liver Enzymes
Serious Potential Hepatotoxic risk
Respiratory failure in Myasthenia Gravis patients
Visual disturbance
Loss of Consiousness

66
Q

When are Ketolides used

A

ONLY WHEN NEEDED
Serious infections that dont respond to anything

67
Q

What are Oxazolidinones

A

New class of Synthetic antibiotics

68
Q

Name an Oxazolidinones

A

Linezolid

69
Q

Spectrum/Uses of Oxazolidnones

A

Gram +ive bacteria (staphylococci, streptococci, enterococci, Gram +ve Anaerobic cocci and Rods)
Cloxacillin-resistant Staphylococci and Vancomycin-Resistant Enterococci, MRSA
Drug resistant M.Tuberculosis

70
Q

Are Oxazolidinones Bacteriostatic or Bactericidal

A

Mostly bacteriostatic
*Bactericidal against Streptococci

71
Q

When should the Oxazolidinones be used

A

As last resort where other Antibiotic therapy has failed–> should be reserved for this purpose

72
Q

MOA of Oxazolidinones

A

Prevents formation of Ribosomal COmplex
Binds to 23S subunit of 50S subunit =inhibits Protein Synthesis

73
Q

Admin of Oxazolidinones

A

IV or oral, 100% bioavailable

74
Q

Resistance mechanism against Oxazolidinones

A

Mutation of Linezolid binding site on 23S ribosomal subunit

75
Q

SEs of Oxazolidinones

A

Hemolytic toxicity: mild & reversible
Peripheral Neuropathy: prolonged use
Reversible non-selective inhibitor of MAO
Headache
Moniliasis/fungal infection
Metalic taste
GIT effects
Neurotoxicity

76
Q

DIs of Oxazolidinones

A

Sympathomimetic or Adrenergic drugs
–>produce Serotonin Syndrome: fever, flushing, sweating, tremors, delirium

77
Q

What are Streptogramins

A

Semisynthetic derivatives of Pristinamycin: which is a naturally occurring STreptogramin

78
Q

Name the Streptogramins

A

Quinupristin-Dalfopristin: fixed 30/70

79
Q

Effect of combined Streptogramins

A

Synergistic
Each agent alone: bacteriostatic
Combined: Bactericidal

80
Q

Spectrum/uses of Streptogramins

A

Most Gram +ive bacteria and most respiratory pathohens
90% Stap. aureusa and Coagulase neg. Staphylococci incl MR strains
Penicillin resistanct Pneumococci
Enterococcus Faecium incl. strains which are resistant to Ampicillin, Genatmicin and Vancomycin

81
Q

MOA of Streptogramins

A

bind to distant sites o 50S subunit–> interfere with Peptidyl Transferase enzyme

82
Q

Resistance mechanism against Quinuprostin

A
  1. A ribosomal methylase that prevents binding
  2. Lactonase produced that inactivates the drug
83
Q

Resistance Mechanisms against Dalfopristin

A

Acetyltransferase produced that inactivates drug
–> incr. efflux of drug

84
Q

Admin of Streptogramins

A

IV: rapid metabolism

85
Q

Effect of Streptogramins on Liver enzymes

A

inhibit CYP3A4–> DIs

86
Q

SEs of Streptogramins

A

Inflammation, pain, Oedema, infusion site rxn, Thromophlebitis
NVD
Rash, purirtis
Headache
Pain
Athralgia and Myalgia
Asthenia
Conjugated Hyperbilirubinaemia

87
Q

DIs of Streptogramins

A

Warfarin
Diazepam
Terfenadine
Astemiazole
Cisapride
NNRTI
Cyclosporine
–> inhibition of their metabolism

88
Q

What is a Lipopeptide

A

naturally occurring compound found in soil of Streptomyces Roseosporus

89
Q

Name a Lipopeptide

A

Daptomycin: IV

90
Q

Spectrum/Uses

A

infections caused by multi resistant bacteria
Active against Gram +ive bacteria only
MRSA
Glycopeptide Resistant enterococci
Skin and skin structures infections: gram +ive
S.aureus bacteriaemia incl. right-sided infective Endocarditis

91
Q

MOA of Lipopeptides

A

Disrupting bacterial cell membrane function
Bind to membane and cause rapid depolarisation
Cause a loss of membrane potential
inhibition of protein, DNA and RNA synthesis
Bactericidal: depends on conc.

92
Q

SEs of Lipopeptides

A

CVS, CNS SEs
Rash
GIT effects
Electrolyte disturbance
Hematological, musculoskeletal and hepatic effects
Hypersensitivity rxns
Possible myopathy and Rhabdomyolysis with statins

93
Q

Drugs that cause Disruption of Bacterial Plasma Membrane

A

Polymyxin B and E(Colistin)

94
Q

MOA of Polymyxin B and E

A

attach to Phospholipids in bacterial plasma membrane–> disrupt membrane structure
Change membrane permeability
Selective bactericidal to Gram -ive bacteria

95
Q

Admin of Polymyxin B

A

Topical use only in combination with other agents

96
Q

Spectrum/Uses of Polymyxin B

A

Skin, eye, ear infections

97
Q

When is IV Polymyxin used

A

combination salvage therapy in exceptional cases of infections due to multi-drug resistant gram -ive pathogens (p.aeuroginosa, Actinobacter baumanii)

98
Q

SEs of Polymyxin

A

Parentral: nephrotoxic and neurotoxic

99
Q

Admin of Polymyxin E(colistin)

A

IV, combination therapy

100
Q

Spectrum/Uses of Colistin

A

Severe Resistant Gram -ive infections (carbapenems resistant)
Last line treatment for Multi-drug resistant infections

101
Q

SEs of Colistin

A

Reversible Nephrotoxicty

Pharmacology (50 decks)

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