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Pharm > Pharm Anti-infective agents > Flashcards

Pharm Anti-infective agents Flashcards

1
Q

Classifications of bacteria

A
  1. spheres/cocci
  2. rods/bacilli
  3. spirals
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2
Q

Gram + or - staining process

A
  1. Fixation
  2. Crystal Violet
  3. Iodine Treatment
  4. Decolorisation
  5. Counter stain with Safranin
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3
Q

Gram + structure

A

Gram +:
* Cell wall thick multilayered Peptidoglycan outside of cytoplasmic mem

Gram -:
* single layered Peptidoglycan within periplasmic space
* Outer membrane= Lipopolysaccharide which prevents penetration of Gram stain

Penicillin binding proteins: found in both and strengthen peptidoglycan
Beta lactamases: chew up penicillins and cephalosporins

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4
Q

Gram + overview of bacteria

A
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5
Q

Gram - overview of bacteria

A
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6
Q

Misc bacterial inf

A

intracellular bacteria
* chlamydia
* rickettsia
* borellia

Poorly staining
* mycoplasma
* legionella
* helicobacter

Acid fast stain
* mycobacteria
* nocardia
* tuberculosis

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7
Q

Bacterial Growth stages

A
  1. Lag phase- adapt to environ, synthesis
  2. Log phase- doubling per unit time MOST SUSCEPT TO AB bc so fast
  3. Stationary phase- nutrient depletion, accumulation of byproducts
  4. Death phase- starvation
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8
Q

Chemotherapy

A

anticancer tx antibiotics= chemotherapy

BOTH TARGET RAPIDLY DIVIDING CELLS

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9
Q

Antibiotics come from?

A
  • derived from natural biologic products ie environ competing organisms-> fungi
  • daily= organisms exposed to these agents in small amounts
  • we give significant doses and have consequences= resistance
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10
Q

Ampicillin does work on me?

A

Agents are specific to microbes not people
* idiosyncratic pharmacokinetics and enzyme induction does differ
* mostly= its bc agents are prescribed indiscriminantely

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11
Q

Choosing a drug

A
  1. Host Factors- liver/kid fxn, allergies, age, prego, exposures
  2. Drug factors- pharmacodynamics, kinetics, tissue penetration, toxicities
  3. Bug factors- possible resistance patterns, duration of disease, likelihood of multiple organisms
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12
Q

Sensitivity testing

A
  1. Zone of inhibition on overnight culture-> Kirby-Bauer Method
    Tells you which AB bug will be sens to
    GET CULTURES B4 DRUG THERAPY
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13
Q

Susceptibility and Resistance

A
  1. Minimum Inhibitory Concentration (MIC)= lowest conc of the AB results in inhibition of visible growth
  2. Minimum bactericidal conc (MBC)= lowest conc of AB that kills 99.% of original
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14
Q

Pharmacokinetics

A
  • Route: oral preferred but IV/IM for very sick, meningitis, endocarditis, N/V
  • Decreased/Increased dosage requirements: Hepatic/Renal, burns, CF, trauma, age, Prego
  • Penetration: CSF inflammation
  • Monitoring: Peak and trough levels= Ththerapeutic index, substantial interpatient variability
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15
Q

Tissue Specificity- Penetration

A
  1. Gut infections= best tx by Oral med- cant be absorbed into body
  2. CNS infections: some dont penetrate BBB
  3. Bone: dependent on molecular size, protein binding, fat solubility
  4. Soft tissues (cellulitis)
  5. Abscesses: no blood flow= poor penetration (must be drained)
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16
Q

Antimicrobial agents: MOA

A
  • target bacterial cell envelope-> cell wall synthesis and cytoplasmic membrane structure= MC MECHANISM
  • Block production of new proteins= bacterial ribosome
  • target DNA or DNA replication= antimetabolite activity
17
Q

Basic mechanisms of resistance

A
  1. Drug inactivation or modification-enzymatic deactivation of Penicillin through production of beta lactamases
  2. Alteration of target site- alt Penicillin binding protein-> binding target site of penicillin MRSA
  3. Alteration of metabolic pathway-sulfonamide-para aminobenzoic acid = folate precursor
  4. Reduced drug accumulation- decreasing drug permeability or increasing active efflux of the drugs across the cell surface
17
Q

Basic mechanisms of resistance

A
  1. Drug inactivation or modification-enzymatic deactivation of Penicillin through production of beta lactamases
  2. Alteration of target site- alt Penicillin binding protein-> binding target site of penicillin MRSA
  3. Alteration of metabolic pathway-sulfonamide-para aminobenzoic acid = folate precursor
  4. Reduced drug accumulation- decreasing drug permeability or increasing active efflux of the drugs across the cell surface
18
Q

MRSA

Methicillin resistant Staph aureus

A

Mech: mutation by penicillin binding protein PBP
now isolates resistant vancomycin, linezolid

19
Q

Alternate Classification of Resistance

A
  1. Natural or intrinsic resistance
    * inaccessibility of the target- lps in gram neg
    * multidrug efflux sys- pumping out multiple drugs
    * drug inactivation= beta lactamase
  2. Acquired resistance= disseminated by plasmids or transposons
    * drug modification
    * drug inactivation- beta lactamase
    * drug efflux
20
Q

When cause is known?

A

interpretation of Culture and Sens-> Monitoring response-> Clinical failures

21
Q

Classifications of Antibiotics

A

Mode of action:
* bacteriostatic
* bactericidal

Spectrum of action
* broad
* narrow

22
Q

Antibacterial agents

A

Bactericidal: active in killing
Bacteriostatic: limit bacterial growth
Organisms can lose susceptibility to certain drugs= direct result of AB overuse

23
Q

Clinical use of AB

A
  1. Initial concerns: clinical findings, clinical specimens, likely organisms, prevention of secondary cases
  2. Next level: spectrum based on culture results, combination therapy, dose, route, duration, clinical response
24
Q

Use of drug combinations

A
  1. Increase spectrum, polymicrobial infections, decrease development of resistance
  2. Synergism: blockade of sequential metabolic steps, enzyme inhibition, enhancement of uptake
  3. Antagonism: statics inhibit cidals, induction of microbial enzyme pathways
25
Q

Prophylaxis

A

Surgery, dentistry
rheumatic fever
HIV
Malaria
secondary contacts
pneumococcus for HbSS or splenectomy
UTIs/OM
Neonates- group B strep

26
Q

Main side effects with Most antibiotics

A
  1. GI side effects-> diarrhea
  2. Type 1 hypersensitivity

Pharm (9 decks)

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