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CD 09 Flashcards

(46 cards)

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1
Q

Erythromycin commomnly cause GI disturbances ?

A

True

Azithromycin Clarithromycin better tolarated

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2
Q

Gentamycin is not active when given orally

A

All aminoglycosides are needed to given IV or IM route. Because they can not absorb from the GI tract and so given Parenterally.

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3
Q

Ciprofloxacin interects with theophylline used for asthma management

A

True. cpro inhibits hepatic metabolism of theophylline and increase its toxicity

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4
Q

Tetracycline should be avoided in pregnency and in your children

A

True, Tetracycline chelate Ca2+ and cause disclolouration of growing teeth

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5
Q

What are the selective drug target of a bacteria

A
  • Bacterial cell wall

- Cell membrane

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6
Q

Structure of Gram Negative Bacteria is a bit complex which has

A
  • Inner membrane
  • Peptidoglycan (Cell wall)
  • Outer Membrane
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7
Q

The sturecture of Gram positive is a bit simple it has

A
  • Inner membrane

- Peptidoglycan

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8
Q

What is bacteria peptidoglycan (murein) has

A

A 3D meshwork of peptide cross linked sugar polymers

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9
Q

Why bacterial cell wall has peptidoglycan?

A

Peptidoglycan (Murin) Is important for bacterial survival

It gives rigidity and structure to the bacteria, so that, it can protect against osmotic gradient so they don’t burst.

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10
Q

How Peptidoglycan biosynthesis work?

A
  1. Cytoplasm (Synthesis of Murein monomers) =>
  2. Membrane (export to the inner membrane and flipped externally)=>
  3. Then peptidoglycan polymer cross-linking of glycan strands.
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11
Q

What is beta lactams common

A

The RING is the common but the other group attached to the ring is quite unique. Those Unique sturcture around the ring gives different spectram of activity

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12
Q

MoA of Beta lactams

A
  1. Inhibit peptidoglycan (As a result no cross-linking)
  2. Target penicillin-binding proteins (PBPs)

All bacteria have several PBPs i.e E.coli has at least 7 PBPs which helps to maintain the rod-like shape of E.coli. Beta-lactam
Inhibit septum formation as a result of no division or lysis.

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13
Q

Several Factors influence the activity of beta lactams those are?

A
  1. Resistance
  2. Enzymatic destruction i.e Beta lectamase enzyme from bacteria, distroy the beta lectam ring of the drug.
  3. Biofilms (Biofilms Produce more polysaccharide as a result hard to penetrate.)
  4. Density and age of infection.
    Need higher con and longer for older infaction, coz they might have more resistance bacteri,or those bacteria can make more beta lectamase enzyme.
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14
Q

Penicillins (ampicillin, amoxicillin, flucloxacillin) cidal or static?

A

BacteriCidal

-Frequently administered with beta lactamase inhibitor (clavulanic acid, sulbactam)

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15
Q 
Clavulanic acid (poor intrinsic antimicrobilal activity)
Combined with amoxicillin (Augmentin)
A
  • “Suicide” inhibitor
  • Irreversibly binds to beta lactamases
  • Oral, also parenteral
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16
Q

Penicillins

e.g. ampicillin, amoxicillin, flucloxacillin

A

-BacteriCIDAL

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17
Q

Pharmacokinetics of Penicillins

e.g. ampicillin, amoxicillin, flucloxacillin

A

Given orally
Excreted by urine
t1/2 short (30-60mins)

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18
Q

Unwanted effects of Penicillins

e.g. ampicillin, amoxicillin, flucloxacillin

A

Hypersensitivity (1-10%)
GI (kill to gut flora) diarrhoia
Rash

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19
Q

Clinical Use of Penicillins

e.g. ampicillin, amoxicillin, flucloxacillin

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A
  • Upper Respiratory Tract Infactions(URTIs)

- Meningitis

20
Q

What are the class of drugs in Cephalosporins?

```
cephalexin 1st generation),
cefaclor (2nd gen),
ceftriaxone (3
rd gen),
cefepime
4th gen
~~~

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A

Similar MoA to penicillins

-But more resistance to Beta lactamase

21
Q

Why do Cephalosporins have developed different Generations?

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A
  • Increased activity for Gram -,
  • Increased BBB penetration,
  • longer t 1/2
22
Q

Pharmacokinetics of Cephalosporins ?

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A
  • oral administration

- Renal excretion

23
Q

What are the Unwanted effects of Cephalosporins?

```
cephalexin (1st gen),
cefaclor (2nd gen),
ceftriaxone (3
rd gen),
cefepime
4th gen
~~~

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A

Similar to penicillins.
Hypersensitivity
Anaphylaxis, bronchospasm, urticarial
Antibiotic associated colitis

24
Q

What are the Clinical useas of Cephalosporins?

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A

-Skin, soft tissue infections
-Pneumonia
-Hospital acquired (nosocomial)
infections

25
What are the Carbapenems class of drug?
E.g. imipenem, meropenem, ertapenem are what spectram ? | Broader spectrum
26
MoA of Carbapenems | E.g. imipenem, meropenem, ertapenem
Similar to Penicillin 1. Inhibit peptidoglycan (As a result no cross-linking) 2. Target penicillin-binding proteins (PBPs) All bacteria have several PBPs i.e E.coli has at least 7 PBPs which helps to maintain the rod-like shape of E.coli. Beta-lactam Inhibit septum formation as a result of no division or lysis.
27
What is the Pharmacokinetics of | Carbapenems? E.g. imipenem, meropenem, ertapenem
- Imipenem not absorbed orally. Once daily dose. - Renal excretion, T half is short - Rapid hydrolysis
28
Unwanted effects of Carbapenems | E.g. imipenem, meropenem, ertapenem
``` Similar to other b lactams Nausea and vomiting Neurotoxicity, seizures (high doses, renal failure, CNS injury/disease) ```
29
Clinical Use of Carbapenems | E.g. imipenem, meropenem, ertapenem
* Septicaemia (a kind of blood infection) | * Hospital-acquired pneumonia
30
Why Some antibiotics are less active against Gram - bacteria than Gram +
Because G- Bacteria has complex cell wall where the antibiotics sometimes can not penetrate on the other hand Gram positive bacteria has simple structure
31
Narrow spectrum
Limited to specifct microbe families
32
Broad spectrum
Extensive, Effective agains Gram positive and Gram negative both.
33
What is peptidoglycan in the cell wall of a bacteria
A 3D meshwork of peptide cross linked sugar polymers | -Bacteria use for survival.
34
For Gram positive bacteria the peptidoglycan how much thick ?
Peptidoglycan is 50 to 100 molecules thick
35
For Gram-Negative bacteria, the peptidoglycan how much thick?
Peptidoglycan is 1 to 2 molecules thick or 5-10nm thick.
36
What is Beta lactamase inhibitor
1.Clavulanic Acid combined with amoxicillin (Augmentin) Irreversibly binds to Beta-lactamase Oral and parenteral 2. Sulbactam combined with ampicillin. Oral and parenteral
37
Beta lactamases inhibitors are mostly active against
Plasma encoded beta-lactamases. | Not active against (Type 1 chromosomal Beta lactamases induced gram-negative bacteria).
38
What are the Monobactams (monocyclic Beta lactams) ?i.e Aztreonam
Mechanism, Unwanted effect and pharmacokinetisc are similar like beta lactams. But only work for Gram negative bacteria.
39
What are the Indications of Monobactams ?
- Only work against Gram negative bacteria and its infection | - influenza
40
What is the Glycopeptides group of drugs do? | i.e Vancomycin, teicoplanin, daptomycin
Bactericidal | Active against G positive bacteria (MRSA)
41
T half of Glycopeptides i.e Vancomycin, teicoplanin, daptomycin
Poor oral absorption. Teicoplanin i.v infusion 8 hours, Renal excretion Dose adjustment required otherwise renal impairment For vencomycin required monitoring to minimize toxicity.
42
Unwanted effects of Glycopeptides i.e Vancomycin, teicoplanin, daptomycin
Nephrotoxicity. Rash Red man syndrome
43
Clinical use of Glycopeptides | i.e Vancomycin, teicoplanin, daptomycin
MRSA | Bacterial endocarditis.
44
What are the killing charecterstics of antibiotics?
- "time oriented killing" (so the drug remains to above Minimum Inhibitory Con for a certain time to kill the bacteria ) i.e Beta lactams - "concentration-dependent killing"(Concentaration is higher the MIC is the important for this drugs) i.e Aminoglycosides - both dependent killing i.e quinolones.
45
Post Antibiotic effect
Suppression of bacterial growth after antibiotics exposure. Strongly work = mainly con dependent drugs.i.e Aminoglycosides. Moderately work=Mainly time dependent drugs. i.e carbapenems,quinolone,Glycopeptides. Weakly work =Drug acting at some critical point in the bacterial reproductive cycle. i.e B-lectams, Cephalosporins Monobactams.
46
Why we need to dose adjustment in patients with renal dysfunction
Patients with kidney disease may have alteration in protein binding,volumes of distribution, kidney clearance and nonreanal clearance. & To prevent accumulation of drug in liver and other body organs as low clearance and to prevent toxicity.
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