Lec2 Flashcards

(56 cards)

1
Q

Drugs that inhibit bacterial protein synthesis

A

1.Macrolides
2.clindamycin
3.tetracyclin
4.aminoglycosides

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2
Q

Macrolides examples

A

1.Erythromycin 2.clarithromycin 3.Azithromycin

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3
Q

Macrolides mechanism of action

A

Bacteriostatic
Inhibit 50s ribosome subunit -> lead to misreading of mRNA->Inhibit bacterial protein synthesis

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4
Q

Macrolides root of administration

A

Oral

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5
Q

Erythromycin distributes well to all body fluid except…….

A

CSF

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6
Q

Root of excretion for erythromycin and azithromycin

A

In the Bile as active drugs

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7
Q

Erythromycin may used as a replacement for penicillin why?

A

It’s used for patient who have penicillin allergy Cuz It’s effective against many of the same organisms as penicillin

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8
Q

When does the erythromycin is used?

A

In gastroparesis cuz it promotes gastric emptying

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9
Q

Drug has the same effect as erythromycin and also effective against haemophilus influenza

A

Clarithromycin

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10
Q

Proffered therapy for urethritis caused by chlamydia trachomatis

A

Azithromycin

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11
Q

Adverse drug reactions of macrolides

A

-GIT upset nausea, vomiting, abdominal pain & diarrhoea
-ototoxicity: associated with erythromycin, especially at high dose

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12
Q

Contraindications of macrolides

A

It can accumulate in the liver in the patient who have hepatic failure

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13
Q

Drug to drug interaction of macrolides

A
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14
Q

Clindamycin mechanism of action

A

Same as macrolides

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15
Q

Root of administration of clindamycin

A

IV & oral-limited by gastrointestinal tolerance-

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16
Q

Distribution of clindamycin drugs in the body

A

Well in all body fluid and boon, poor entry into the CSF

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17
Q

Clindamycin root of excretion

A

Bile

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18
Q

Accommodated clindamycin occur in

A

Severe renal impairment or hepatic failure

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19
Q

Clindamycin used against….

A

Gram positive organisms, including MRSA and streptococcus, and anaerobic bacteria

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20
Q

Adverse drug reactions to clindamycin

A

1.Skin rashes
2 Diarrhea, which may represent a serious pseudomembranous colitis caused by overgrowth of C. difficile.

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21
Q

C. Difficile treatment

A

Oral vancomycin

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22
Q

Tetracyclines examples

A

Doxycycline or tetracycline

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23
Q

Mechanism of action

A

It has the same effect as macrolides but it bind to the 30s subunit of bacterial ribosome not the 50s subunit

24
Q

Root of administration of tetracycline

25
Distribution of tetracycline antibiotics
Penetration into most body fluids is adequate , cross the placental barrier and concentrate in fetal bones and teeth
26
Root of elimination of tetracyclines antibiotics
Primarily in urine but doxycycline eliminated via the bile
27
Which drug is preferred in tetracycline for renally compromised patients
Doxycycline (excretion via bile into the feces)
28
Adverse drug effects of tetracyclines
Gastric discomfort -commonly via irritation of the gastric mucosa. Phototoxicity -if exposed to ultraviolet rayes Vestibular dysfunction -dizziness,vertigo and tinnitus
29
Contraindications of tetracycline antibiotics
Don’t se if -pregnant -breast-feeding Women -less than 8 years of age
30
Aminoglycoside examples
Streptomycin, amikacin or gentamicin
31
Mechanism of action for Aminoglycosides
Same as tetracycline
32
Root of administration of Aminoglycosides
IV or IM
33
Distribution of Aminoglycosides in the body
Poor penetration to CSF also it has a good entry to inflamed tissues
34
Root of excretion
Via glomerular filtration
35
Adverse drug effect for Aminoglycosides
Nephrotoxicity ototoxicity (due to auditory or vestibular nerve damage)
36
Drug to drug interactions for Aminoglycosides
Ototoxicity is enhanced by loop diuretics(e.g.furosemide)
37
Drugs that inhibit bacterial nucleic acid synthesis
1. Quinolones 2. Rifampcin
38
Quinolones examples
Levofloxacin ciprofloxacin
39
Mechanism of action of quinolones
Bactericidal Inhibit DNA gyrase (bacterial topoisomerarse||)-> relaxation of supercoiled DNA(promoting DNA strand breakage) -> inhibit bacterial nucleic acid synthesis
40
DNA gyrase
DNA gyrase : preserve the state of supercoiling in replicating and non-replicating bacterial chromosomes )
41
Distribution of quinolones drug in the body
Distribute well in all body fluids and tissues
42
Root of excretion for quinolones
Renally (dosage adjustment is needed in cases of renal failure)
43
Adverse drug effect for quinolones
-Phototoxicity (if exposed to uv) -Tendinitis or tendon rupture
44
Drug to drug interactions for quinolones
Inhibit hepatic drug metabolism & prolong action of theophylline and warfarin
45
Rifampcin mechanism of action
Bactericidal Inhibit the DNA-dependant RNA polymerase of mycobacterium TB-> prevent transcription of DAN into mRNA
46
Why rifampicin has no effect in some of the mycobacteriumTB
The mycobacterium TB become resistant to the drug because of a mutation in it’s DNA-dependant RNA polymerase gene
47
Root of administration for Rifampicin
Oral
48
Distribution of
49
Distribution of the rifampicin in the body
Widely distributed to all body fluids and organs(including the CSF)
50
Potent liver enzymes inducer
Rifampicin
51
Root of elimination
Primarily through the bile and into the feces a small percentage is cleared in the urine
52
Adverse drug effect of rifampicin
-Red-orange secretions ( tears – urine -....) -Thrombocytopenia -Hepatotoxicity (Hepatitis)
53
Drug to drug interactions of rifampicin
Hepatic enzyme inducer: increase metabolism of warfarin, phenytoin, oral contraceptive pills
54
Antibiotics antagonism
indicates that decreased anti-microbial effect of a drug when combined with another, leading to decreased response
55
Mechanisms of antagonism include:
-Decreased bactericidal activity by bacteristatic agent e.g. tetracycline and Penicillins -Increased enzymatic inactivation e.g. ampicillin decrease pipracillin activity
56
Rule of right (5 Rs)
1.right drug 2. Right dose 3. Right route 4. Right time (interval and duration) 5. Right patient