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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
Chloramphenicol is reserved for
severe infections by susceptible organisms due to potential to cause aplastic anemia
26
Spectrum/Uses of Chloramphenicol
Rickettsial infections: standard drugs CIed Bacterial meningits: standard drugs CIed Typhoid fever Bacterial eye infections: topical
27
Chloramphenicol is active against
Chlamydia Mycoplasma infections Streptococci Staphylococci Hemophilus infections Anaerobes
28
MOA of Chloramphenicol
powerful inhibitor of Protein Synthesis Attaches reversibly to 50S subunit--> interferes with MOA of Peptidyl transferases
29
MOA of Peptidyltransferase
catalyses formation of peptide bind btwn growing peptide and new AA =peptide cant grow further
30
Resistance mechanism against Chloramphenicol
Production of Chloramphenicol Acetyltransferase that inactivates the drug
31
Admin of Chloramphenicol
Chloramphenicol succinate: parenteral --> highly water soluble where it gets hydrolysed to free Chloramphenicol
32
Distribution of Chloramphenicol
widely distributed *high levels in brain and CSF: effective against meningitis
33
Metabolism of Chloramphenicol
in liver and after Glucuronide formation its excreted in urine
34
SEs of Chloramphenicol
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
35
GREY BABY SYNDROME is characterised by
abdominal distention cyanosis vasomotor collapse Failure to feed
36
DIs with Chloramphenicol
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
37
Cautions in Chloramphenicol
Impaired hepatic function Bone marrow depression: cancer, HIV patients
38
CIs of Chloramphenicol
Allergy Porphyria 3rd trimester of pregnancy Neonates Lactation
39
Spectrum/Uses of Clindamycin
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
40
Clindamycin is inactive against
Enterococci
41
MOA of Clindamycin
Inhibits protein synthesis by: binds to 50S subunit--> interferes with formation of initiation complex--> inhibits translocations
42
Different dosages of Clindamycin cause
Low: Bacteriostatic High: Bactericidal
43
Resistance mechanisms against Clindamycin
Mutation of ribosomal binding site enzymatic inactivation
44
Admin of Clindamycin
Oral, IV, IM *taken with adequate fluid to prevent ulceration
45
Metabolism and Excretion of Clindamycin
M; liver E: mainly in bile, small unaltered amount in urine
46
Distribution of Clindamycin
widely distributed *doesn't enter CSF
47
SEs of Clindamycin
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
DIs with Clindamycin
COC
49
Caution in Clindamycin
GIT disease severe hepatic impairment porphyria elderly pregnancy/lactation
50
What is Fusidic Acid
Steroid antibiotic thats usually given Orally/Topically
51
Spectrum/Uses of Fusidic Acid
Severe Staphylococcal infections Combine with Cloxacillin (antistaphylococcal) to prevent emergence of resistance Topically: acute skin infections (5days) and conjunctivis
52
SEs of Fusidic Acid
Reversible Hepatotoxicty GIT effects: take with meals Kernicterus risk in Neonates AVoid in Pregnancy IM: local tissue necrosis Local Hypersensitivity rxns
53
DIs of Fusidic acid
Hydrocortisone: decr. Antibiotic activity and reduced efficacy of Fusidic acid Statins: incr. risk of Rhabdomyolysis
54
CIs of Fusidic Acid
Hepatic Dysfunction: as its excretd in bile
55
Spectrum of Mupirocin
Gram +ive ONLY Effective against Methicillin-resistant Stapylococcal aureus (MRSA)
56
MOA of Mupirocin
Reversibly binds to Isoleusine-tRNA Synthetase and prevents formation of Isoleusine-tRNA -->inhibits protein and RNA synthesis
57
High dosages of Mupirocin results
in Bactericidal effects
58
Admin of Mupirocin
Topical only + intranasal *rapidly inactivated after absorption if given orally
59
SEs of Mupirocin
Mild stinging Burning Itching at site of application
60
Caution in Mupirocin
Porphyria
61
What are Ketolides
Semi-synthetic deruvatives of Erythromycin A--> have broader Spectrum
62
Name a Ketolide
Telithromycin
63
Spectrum/Uses of Ketolides
similar spectrum to macrolides, H.influenzae Erythromycin-resistant strains of Pneumoccoccus
64
MOA of ketolides
Can bind to 2 sites on bacterial ribosome with higher affinity than macrolides *may inhibit formation of newly forming Ribosomes
65
SEs of Ketolides
Inhibit Liver Enzymes Serious Potential Hepatotoxic risk Respiratory failure in Myasthenia Gravis patients Visual disturbance Loss of Consiousness
66
When are Ketolides used
ONLY WHEN NEEDED Serious infections that dont respond to anything
67
What are Oxazolidinones
New class of Synthetic antibiotics
68
Name an Oxazolidinones
Linezolid
69
Spectrum/Uses of Oxazolidnones
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
Are Oxazolidinones Bacteriostatic or Bactericidal
Mostly bacteriostatic *Bactericidal against Streptococci
71
When should the Oxazolidinones be used
As last resort where other Antibiotic therapy has failed--> should be reserved for this purpose
72
MOA of Oxazolidinones
Prevents formation of Ribosomal COmplex Binds to 23S subunit of 50S subunit =inhibits Protein Synthesis
73
Admin of Oxazolidinones
IV or oral, 100% bioavailable
74
Resistance mechanism against Oxazolidinones
Mutation of Linezolid binding site on 23S ribosomal subunit
75
SEs of Oxazolidinones
Hemolytic toxicity: mild & reversible Peripheral Neuropathy: prolonged use Reversible non-selective inhibitor of MAO Headache Moniliasis/fungal infection Metalic taste GIT effects Neurotoxicity
76
DIs of Oxazolidinones
Sympathomimetic or Adrenergic drugs -->produce Serotonin Syndrome: fever, flushing, sweating, tremors, delirium
77
What are Streptogramins
Semisynthetic derivatives of Pristinamycin: which is a naturally occurring STreptogramin
78
Name the Streptogramins
Quinupristin-Dalfopristin: fixed 30/70
79
Effect of combined Streptogramins
Synergistic Each agent alone: bacteriostatic Combined: Bactericidal
80
Spectrum/uses of Streptogramins
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
MOA of Streptogramins
bind to distant sites o 50S subunit--> interfere with Peptidyl Transferase enzyme
82
Resistance mechanism against Quinuprostin
1. A ribosomal methylase that prevents binding 2. Lactonase produced that inactivates the drug
83
Resistance Mechanisms against Dalfopristin
Acetyltransferase produced that inactivates drug --> incr. efflux of drug
84
Admin of Streptogramins
IV: rapid metabolism
85
Effect of Streptogramins on Liver enzymes
inhibit CYP3A4--> DIs
86
SEs of Streptogramins
Inflammation, pain, Oedema, infusion site rxn, Thromophlebitis NVD Rash, purirtis Headache Pain Athralgia and Myalgia Asthenia Conjugated Hyperbilirubinaemia
87
DIs of Streptogramins
Warfarin Diazepam Terfenadine Astemiazole Cisapride NNRTI Cyclosporine --> inhibition of their metabolism
88
What is a Lipopeptide
naturally occurring compound found in soil of Streptomyces Roseosporus
89
Name a Lipopeptide
Daptomycin: IV
90
Spectrum/Uses
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
MOA of Lipopeptides
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
SEs of Lipopeptides
CVS, CNS SEs Rash GIT effects Electrolyte disturbance Hematological, musculoskeletal and hepatic effects Hypersensitivity rxns Possible myopathy and Rhabdomyolysis with statins
93
Drugs that cause Disruption of Bacterial Plasma Membrane
Polymyxin B and E(Colistin)
94
MOA of Polymyxin B and E
attach to Phospholipids in bacterial plasma membrane--> disrupt membrane structure Change membrane permeability Selective bactericidal to Gram -ive bacteria
95
Admin of Polymyxin B
Topical use only in combination with other agents
96
Spectrum/Uses of Polymyxin B
Skin, eye, ear infections
97
When is IV Polymyxin used
combination salvage therapy in exceptional cases of infections due to multi-drug resistant gram -ive pathogens (p.aeuroginosa, Actinobacter baumanii)
98
SEs of Polymyxin
Parentral: nephrotoxic and neurotoxic
99
Admin of Polymyxin E(colistin)
IV, combination therapy
100
Spectrum/Uses of Colistin
Severe Resistant Gram -ive infections (carbapenems resistant) Last line treatment for Multi-drug resistant infections
101
SEs of Colistin
Reversible Nephrotoxicty

Pharmacology (50 decks)

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