Anti-infective Drugs: Module 10 Flashcards Preview

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Flashcards in Anti-infective Drugs: Module 10 Deck (18)
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1
Q

Drug classes in this category

Anti-microbial drugs include:

  • Anti-bacterial’s (antibiotics) used for:
  • Anti-virals used for:
  • Anti-tubercular drugs used for:
  • Anti-mycotics used for:
A
  • Anti-bacterials are for bacterial infections
  • Anti virals for infections
  • Anti-tubercular for tuberculosis (TB)
  • Anti-mycotics for fugal infections
2
Q

When selecting Anti-microbials

  • First:
  • Then determine its susceptibility to various drugs with a?
  • Consider location of?
  • Consider drug?
A
  • first isolate, identify micro-organism by growing a culture
  • culture and sensitivity results take 48 hours
  • Consider location of infections
  • Consider drug cost, adverse effects, patient allergies.
3
Q

Ideally, select agent after organism identified, drug sensitivity established.

  • Treating presumptively if acutely ill, treat while wait for laboratory analysis
  • Treat presumptively with:

If gram-positive only:

If gram-negative only:

If mixed:

If anaerobic only:

A
  • treat presumptively, broad spectrum antibiotic (effective against gram-positive, gram-neg, and anaerobes)
  • gram-pos: continue gram-positive coverage; discontinue gram-neg.
  • gram-neg: continue gram-neg coverage; discontinue gram-pos, anaerobic coverage
  • Mixed: continue therapy as initiated
  • continue anaerobic only; discontinue gram-pos and neg coverage.
4
Q

Antibiotics:

Narrow spectrum:

Broad spectrum

A

Antibiotics: substances derived from one living organism that can kill another organism; used systemically
-Narrow spectrum: act only on single or limited group of microorganisms

-Broad spectrum: affect wide variety of microbial species; more harmful to normal gut flora when taken long-term or repeatedly short-term

5
Q

Medically important microorganisms

A
chlamydia
spirochetes
gram (+) cocci
gram (-) Entric rods
Other Gram (-) bacilli
Gram (-) cocci
Mycoplasma
6
Q

Antibiotic Resistance

-Acquired resistance:

Causes

  • Given unnecessarily:
  • Over use:
  • Broad versus narrow spectrum:
  • Incomplete dosage taken:
A

-Acquired resistance: drug-resistant genes incorporated into bacteria genetic code with each new generation

  • Given unnecessarily: upper respiratory infections
  • Over use: low doses in animal feed
  • Broad versus narrow spectrum: avoid wide spectrum, except in emergency situations
  • Incomplete dosage taken: selects for resistant organisms
7
Q

Antibiotic
-Bacteriostatic:

-Bactericidal:

A
  • Bacteriostatic: temporarily inhibit bacterial growth, giving time for host’s immune system to respond
  • Bactericidal: kill bacteria
8
Q

Antibiotics Mechanisms
-Inhibit:

  • Alter:
  • Inhibit
A

-inhibit cell wall synthesis

  • Alter membrane permeability or active transport mechanisms
  • Inhibit protein synthesis: act on ribosomes
9
Q

Antibiotic Classes
-Penicillins:

  • Cephalosporins:
  • Tetracyclines:
  • Macrolides (Erythromycin)
  • Carbapenems:
  • Fluoroquinolones (Quinolones):
  • Sulfonamides:
A
  • Penicillins: bactericidal; inhibit cell wall synthesis; broad spectrum, beta-lactam molecular structure (penicillin G, amoxicillin
  • Cephalosporins: bactericidal; inhibit cell wall synthesis; beta-lactam molecular structure; 4 generations [cefazolin, cefaclor, cefixime, cefepime]

Tetracyclines: bacteriostatic, inhibit protein synthesis; broad spectrum; 4-ring structure; originally isolated from Streptomyces aureofaciens; bind (chelate) divalent metals (Ca++, Zn++, Mg++) leading to teeth, bone discoloration; requires second form of birth control with use [doxycycline, tetracycline]

Macrolides: bacteriostatic; inhibit protein synthesis; broad spectrum; isolated from Streptomyces aureofaciens [erythromycin, azithromycin]

  • Carbaenems: inhibit bacterial cell-wll synthesis; broadest spectrum available, used for life-threatening, nosocomial (hospital-acquired) infections [imipenem]
  • Fluoroquinolones: bacteriocidal; interrupt DNA synthesis during replication [cliprofloxacin]
  • Sulfonamides: bacteriostatic; inhibit folic acid production ➡ inhibits growth; require adequate fluid intake to prevent stone formation [sulfadiazine, sulfixoxazole]
10
Q

Antibiotics

Cephalosporins incorporates itself?

A

-incorporates itself into cell wall
Inhibit cell wall synthesis

Daughter cells unable to close cell wall as result of cephalosporin leads to cell death

11
Q

Antibiotics

Cephalosporins

  • First-generation:
  • Second-generation:
  • Fourth-generation:
A
  • First-generation: for gram-positive, staphylococcal, streptococcal infections; used for those allergic to penicillin
  • Second-generation: for gram-negative, anaerobic infections
  • Fourth-generation: for gram-positive, gram-negative infections.
12
Q

Anti-viral Drugs
-Viruses:

  • Respiratory infections:
  • Herpes, Cytomegalovirus infections:
  • HIV:
  • Hepatitis, Leukemia, Kaposi’s Sarcoma:
A
  • Viruses: lack cell wall, cell membrane; therefore not affected by antibiotics
  • Respiratory infections: for prevention; may block membrane proteins, interfere with release of new virons [amantadine, rimantadine]
  • Herpes, Cytomegalovirus infections: for acute phase; terminates DNA-chain synthesis [acyclovir, famciclovir]
  • HIV: terminates DNA-chain synthesis [abacavir, zidovudine]
  • Hepatits, Leukemia, Kaposi’s Sarcoma: may iinhibit viral RNA translation [interferon]
13
Q

Anti-viral

HIV Drugs

  • Nucleoside Reverse Transcriptase Inhibitors (NRTIs):
  • Nucleotide Reverse Transcriptase Inhibitors(NtRTIs):
  • Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs):
  • Protease Inhibitors (Pls):
  • Fusion Inhibitors:
A

-NRTIs: inhibit reverse transcriptase➡ DNA chain termination [didanosine, lamivudine, zalcitibine, zidovudine, emtricitabine, abacavir]

  • NtRTIs: inhibit reverse transcriptase ➡ DNA chain terminatio [tenofovir]
  • NNRTIs: bind reverse transcriptase, inhibiting RNA and DNA-directed DNA plymerase functions [delavirine, efavirenz, nevirapine]
  • PIs: bind protease ➡ inhibits virus particles [amprenavir, atazamavor, lopinavir, ritonavir, saquinavir, indinivir]
  • Fusion: denies cell entry [pentafuside]
14
Q

7 steps of HIV Replication

A
  1. HIV virus binds cell receptor
  2. Virus penetrates cell, HIV RNA enters cell
  3. Reverse transcription: single strand viral RNA ➡ double strand DNA by reverse transcriptase enzyme
  4. Viral DNA combined with cell’s DNA by integrase enzyme
  5. Transcription: viral proteins assembled
  6. immature virus emerges from cell
  7. Maturation of functional virus
15
Q

Where HIV Drugs Work

A
  1. HIV virus binds cell receptor
  2. Virus penetrates cell, HIV RNA enters cell
  3. Reverse transcription: single strand viral RNA ➡ double strand DNA by reverse transcriptase enzyme
  • Nucleoside Reverse Transcriptase inhibitors
  • Nucleotide Reverse Transcriptase Inhibitors
  • Non-Nucleoside Reverse Transcriptase Inhibitors
    4. Viral DNA combined with cell’s DNA by integrase enzyme
    5. Transcription: viral proteins assembled

x-Protease Inhibitors

  1. Immature virus emerges from cell

7 Maturation of functional virus

16
Q

Anti-tubercular Drugs

  • Tuberculosis (TB) caused by:
  • Treatment:
  • Requires long-term:
A
  • TB: caused by Mycobacterium tuberculosis; world-wide killer.
  • Treatment not always curative, can halt progression of infection; drugs specific for mycobacteria [isoniazid, rifampid, pyazinamide]
  • Requires long-term medical therapy (6-9 months) = poor patient compliance ➡ drug-resistant TB
17
Q

Anti-mycotics

  • Anti-fungal drugs for:
    - Fungistatic:
    - Fungicdal:
  • Mechanisms:
    - Ampotericin B:

Adverse effect:

A
  • Anti-fungal drugs: for systemic fungal infections (Candida, Aspergillus) [amphotericin B, fluconazole, ketoconazole, nystatin]
    - Fungistatic: inhibits funga lgrowth, multiplication
    - Fungicidal: destroys fungi
  • Mechamisims: disrupt membrane function allowing cell leakage; incorporated in fungal RNA altering protein synthesis
  • Amphotericin B: low therapeutic index, highly toxic

-Adverse Effects: kidney toxicity

18
Q

Anti-mycotics

rhAPC:

  • Anti:
  • Mechanism:

Adverse Effects:

A
  • Recombinant human activated protein C (rhAPC): new drug class, for severe sepsis with high risk of death from acute organ dysfunction [drotrecogin alfa]
  • Anti-thrombotic, anti-inflammatory, fibrinolytic properties
  • Mechanism: unknown
  • Adverse effects: bleeding