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Y2S1-Pharmacology > Drugs used for pneumonia > Flashcards

Drugs used for pneumonia Flashcards

1
Q

What are the drugs that inhibit nucleic acid synthesis?

A

1) Fluoroquinolones

2) Metronidazole

3) Rifamycin

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2
Q

What is vancomycin?

A
  • Glycopeptide antibiotic
  • Used against MRSA and other gram positive bacteria where it is bactericidal
  • It has no activity against gram negative organisms
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3
Q

What is the mechanism of action of vancomycin?

A
  • It inhibits the cell wall synthesis of the bacteria, by blocking the cross-linking of the peptidoglycan wall
  • It does that by binding to the transglycosylases, which will then inhibit the binding of NAM-NAG sugars together
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4
Q

Why is reaching the cell wall of gram-positive bacteria easier than a gram -?

A

Because they do not have an outer layer

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5
Q

How does penicillin differ from vancomycin?

A

Penicillin is way larger, penicillin can get through the lipid bilayer on the other hand vancomycin is three times bigger with a net positive charge, and thus vancomycin cannot enter the gram-negative bacterial cell

  • Also due to the large size of vancomycin limits its oral effectiveness, as it cannot cross the GIT to the blood in an effective amount that is necessary to treat the infection
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6
Q

When is oral vancomycin used?

A
  • Oral vancomycin won’t have the same side effects as the IV one (cytotoxicity, nephrotoxicity, etc)
  • It is used to treat Clostridium difficile infections
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7
Q

Describe the pharmacokinetics of vancomycin

A
  • Poorly absorbed from the GIT
  • Oral administration is only for the treatment of enterocolitis caused by clostridium difficile
  • Widely distributed in the body
  • Adjust dose in renal dysfunction
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8
Q

How does the bacteria develop resistance against vancomycin?

A

By synthesizing a cell wall precursor that ends in the dipeptide (D-Ala-D-Lac) instead of D-Ala-D-Ala, reducing the binding affinity of vancomycin

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9
Q

What are the clinical uses of vancomycin?

A

1) Sepsis or endocarditis caused by MRSA

2) MSSA in patients who are allergic to penicillins or cephalosporins

3) Vancomycin + Gentamicin is an alternative regimen to treat enterococcal endocarditis in patients with penicillin allergy

4) Vancomycin + Cefotaxime or Ceftriaxone is used to treat meningitis (which is caused by a penicillin-resistant strain of pneumococcus)

5) No activity against gram-negative

6) Oral vancomycin for enterocolitis caused by clostridium difficile

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10
Q

What are the adverse effects of vancomycin? (mosh mawgooden bl oral most of them)

A
  • mnemonic (Vancomycin is NOT Recommended)

1) N: Nephrotoxicity (coadministration with aminoglycosides will increase this toxicity)

2) O: Ototoxicity (coadministration with aminoglycosides will increase this toxicity)

3) T: Thrombophlebitis (as it irritates tissue at sites of injection)

4) R: Red-man syndrome (due to histamine release, only in IV given too quickly)

5) Chills and Fever

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11
Q

What is the 4th generation cephalosporin drug (Antipseudomonal cephalosporin)?

A

Cefepime

  • They are antipseudomonal cephalosporins
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12
Q

In which diseases is cefepime used?

A

1) Pneumonia

2) Empiric treatment of febrile neutropenic patients

3) Urinary tract infections

4) Brain abscess

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13
Q

What are the 5th-generation cephalosporins (Anti-MRSA cephalosporin)?

A

1) Ceftaroline

2) Ceftobiprole

  • They are the Anti-MRSA cephalosporin
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14
Q

When is the fifth-generation cephalosporin used?

A

1) MRSA

2) Vancomycin-resistant staphylococcus aureus (VRSA)

1) Ceftobiprole:

  • Hospital-acquired pneumonia (HAP)
  • Community-acquired pneumonia (CAP)

2) Ceftaroline:

  • Community-acquired pneumonia (CAP)
  • Complicated skin and skin structure infections
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15
Q

Which drug is used in hospital-acquired pneumonia?

A

Ceftobiprole

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16
Q

Which drugs are used in community-acquired pneumonia?

A

1) Ceftobiprole

2) Ceftaroline

17
Q

Describe the pharmacokinetics of the 5th-generation cephalosporins

A
  • (Ceftaroline fosamil) and (ceftobiprole medocaril) have enhanced gram-positive activity, especially their ability to bind to MRSA and penicillin-resistant S.pneumonia
  • Both of them are active against VRSA
  • Their parenteral preparation is a prodrug, which is rapidly converted to ceftaroline on an IV administration
18
Q

What are the different nucleic acid inhibitors?

A

1) Quinolones

2) Fluroquinolones

3) Antifolates

19
Q

What is the first generation of nuclein acid inhibitors?

A

Quinolones

20
Q

What are the different quinolone drugs?

A

1) Nalidixic acid (dr mentioned)

2) Cinoxacin

21
Q

What is the second generation (till the fourth) of nucleic acid inhibitors?

A

They are the fluoroquinolones

  • It is created by adding a fluorine atom to quinolones
  • They had a broad antimicrobial activity after oral administration
  • The suffix “floxacin” signifies the fluorine atom
22
Q

What are the drugs of the second generation of fluoroquinolones?

A

1) Ciprofloxacin (first line for pneumonia by pseudomonas, they kill all gram -ve bacillim, dr mentioned)

2) Norfloxacin (dr mentioned)

3) Ofloxacin (dr mentioned)

4) Enoxacin

5) Pefloxacin

6) Lemofloxacin (dr mentioned)

23
Q

What are the third-generation drugs of fluoroquinolones?

A

1) Levofloxacin (Instead of killing all gram -ve bacilli is will change the “pseudomonase, a gram -ve, with streptococcus, a gram +ve”) dr mentioned)

2) Sparfloxacin

3) Grepafloxacin

24
Q

What are the fourth-generation drugs of fluoroquinolones?

A

1) Trovofloxacin

2) Moxifloxacin (dr mentioned)

3) Gatifloxacin (dr mentioned)

4) Gemifloxacin (dr mentioned)

25
Q

What is the mechanism of action of the quinolones and fluoroquinolones?

A
  • The first generation is not used anymore
  • They act on the nucleic acid of the bacteria, inhibiting their synthesis, By inhibiting DNA gyrase “mainly for gram-negative” and Topoisomerase IV “mainly for gram-positive”, the supercoiled of the DNA won’t be relived (which is the normal function of these enzymes), which will result in the cessation of DNA replication, DNA damage, and ultimately bacterial cell death.
  • Bacteria have topoisomerase IV while humans have topoisomerase 2 + humans no gyrase
  • They are toxic in high doses
26
Q

What are the subclasses of antifolates?

A

1) Sulfonamide

2) Dihydrofolate reductase (DHFR) Inhibitor

27
Q

Which generation of nucleic acid inhibitors are the respiratory fluoroquinolones?

A

Mnemonic جمل:

1) Levofloxacin

2) Gemifloxacin

3) Moxifloxacin

28
Q

What was the first quinolone made used for?

A

UTI

29
Q

Which drug had a good oral antimicrobial effect?

A

Fluoroquinolones

  • But some had fatal side effects (like phototoxicity, QTc prolongation, hypoglycemia, cardi, and hepato-toxicities)
30
Q

How can a bacteria develop resistance against quinolones and fluoroquinolones?

A

If a mutation in the gene that encodes the A subunit of the gyrase occurs

31
Q

Fluoroquinolones are active against which bacterial specimen?

A

1) Proteus

2) E.coli

3) Klebsiella

4) Salmonella

5) Shigella

6) Enterobacter

7) Campylobacter

8) Some are active against pseudomonas saprophyticus (ciprofloxacin, levofloxacin)

32
Q

Ciprofloxacin which generation and which bacterial species does it kill?

A
  • The second generation, it kills all gram -ve bacilli:

1) E.coli
2) Klebsiella
3) H.influenza
4) Proteus
5) Pseudomonas

6) They also target some atypicals

  • First-line treatment for pneumonia due to pseudomonas
33
Q

Which bacteria do levofloxacin & moxifloxacin target?

A
  • Third generation & fourth generation respectively, it targets:

1) Streptococcus (Gram +ve)

all gram negative except pseudomonas:

2) E.coli
3) Klebsiella
4) H.influenza
5) Proteus

6) Atypicals

34
Q

What are the mechanisms by which bacterial resistance occur?

A

1) Mutations in chromosomal genes

  • In genes that encode the DNA gyrase and topoisomerase IV
  • Or regulate the expression of cytoplasmic membrane efflux pumps (altered permeation mechanism)

2) Major plasmid-mediated resistance mechanism

  • Qnr proteins (plasmid-encoded, which protects the DNA gyrase and topoisomerase IV from inhibition by quinolones)
  • Fluoroquinolone-modifying enzymes (they acetylated fluoroquinolones reducing their activity)
  • Efflux pump which will pump fluoroquinolone out of the cell
35
Q

Describe the pharmacokinetics of nucleic acid inhibitors

A

1) Most quinolones are well absorbed orally

2) Quinolones have a high distribution volume

3) They are excreted by the kidneys except for moxifloxacin

4) Moxifloxacin should not be used in patients with hepatic failure

5) They can be given orally, by IV, and even as eye drops

36
Q

What are the adverse effects of quinolones?

A
  • GI:

1) Nausea

2) Vomiting

3) Abdominal discomfort

4) Fluoroquinolones can cause colitis due to clostridium difficile (then give vancomycin)

  • Neuro:

1) Headache + dizziness

2) Convulsion (especially in patients with epilepsy)

3) Peripheral neuropathy (rarely induced by fluoroquinolones)

  • MSK:

1) Tendinitis

2) Arthralgia

  • Other:

1) Moxifloxacin (highest risk for QTc prolongation)

2) Gatofloxacin (induces both hyper and hypoglycemia)

3) Rashes

37
Q

Which fluoroquinolone can induce both hypo and hyperglycemia?

A

Gatifloxacin

38
Q

Which fluoroquinolone has the highest risk for QTc prolongation?

A

Moxifloxacin

39
Q

What are the drug-drug interactions of nucleic acid inhibitors?

A
  • They form complexes with (calcium, iron, aluminum, etc), where if those ions are coadministered with them it will reduce their bioavailability, lazem 2hr separation
  • Ciprofloxacin will increase the bioavailability of theophylline by inhibiting CYP1A2, which might lead to toxicity
  • Cautios with patients taking antiarrhythmic (due to QTc prolongation)

Y2S1-Pharmacology (10 decks)

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