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Integ Exam 1 > Antibiotics and Antifungal Agents Lecture > Flashcards

Antibiotics and Antifungal Agents Lecture Flashcards

1
Q

Classification by MOA

A

Inhibitors of cell wall synthesis
Protein synthesis inhibitors
Inhibitors of nucleic acid function or synthesis
Inhibitors of cell membrane permeability/function

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2
Q

Factors affecting drug choice and drug activity

A 
ID and drug sensitivity of the organism
Status of host defenses/immune function
Bacteriocidal vs bacteriostatic MOA
Antimicrobial resistance
Site of infection
Absorption, Distribution and pharmacokinetics issues
Metabolism and elimination pathways
Pharmacogenetics of the host
Drug interactions
Pregnancy or nursing infants
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3
Q

ID and drug sensitivity of the organism

A

Best educated guess, based on history and clinical exams

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4
Q

Empiric therapy

A

Decision based on population parameters and statistics

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5
Q

Definitive therapy

A

Decision based on ID and lab study of specific organisms in the patients

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6
Q

Status of host defenses/immune function

A

Good host immune system function is critical in synergy with the antibiotic agent for successful therapy

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7
Q

Bacteriocidal vs bacteriostatic MOA

A

Some antibiotics kill the bug, some only inhibit its active growth

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8
Q

Antimicrobial resistance

A

Creates a selective survival advantage for certain individual organisms present
Resistance may be aquired or intrinisic
Transfer can be vertically or horizontally
May develop rapidly

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9
Q

Site of infection

A

Reduced drug deliviery relative to plasma
Local factors: pH, low oxygen levels
Foreign Bodies: catheters, artificial joints

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10
Q

Absorption, distribution and pharmacokinetics issues

A

Desire prompts delivery

Reach peak plasma concentration 1-2 hours after PO administration

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11
Q

Metabolism and elimination pathways

A

May accumulate to toxic levels if elimination pathways are compromised

  • Renal disease: lower excretion
  • Hepatic disease: lower metabolism
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12
Q

Pharmacogenetics of the host

A

Population differences in metabolism are due to genetic variation

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13
Q

Pregnancy and nursing infants

A

Potential for toxic or teratogenic effects of fetus

Alter normal flora of newborns or create allergies

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14
Q

Six P’s of Resistance

A 
Penetration
Porins
Pumps
PBP's
Penicillinase
Pathway/Process
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15
Q

Penetration

A

Cannot pass into human cells, then it cannot cause a reaction and get rid of the infection
- Atypical organisms move into the cell and live there

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16
Q

Porins

A

Channels

Drugs must make its way through these in order to get rid of the infections

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17
Q

Pumps

A

Efflux pumps

Push a drug into the bug and is pumped straight back out –> Never achieves effect concentration (MIC)

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18
Q

PBP’s

A

Altered receptors –> Less effective

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19
Q

Penicillinase

A

Can be upregulated so it will chew up the penicillin

  • Microorganism is making an enzyme that is rendering the drug in effective (chew it up)
  • Enhanced inactivation of drug
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20
Q

Pathway/Process

A

Get around the affect of the organisms, it diverts to another pathway to accomplish the same thing

21
Q

Complications of treatment?

A

Development or emergence of resistance
Therapy fails from outset (not sensitive to the drug)
Drug interactions/antagonism or PK (patient genetics)
Hypersensitivity
Direct toxicity to the host
Superinfections (overgrowth)

22
Q

What is superinfection?

A

Appearance of a new infection by different organisms
Dangerous bc organisms is difficult to eradicate
Caused by a removal of inhibition by normal flora
Frequent with prolonged antibiotic use

23
Q

Tetracycline, Minocycline, Doxycycline, Gentamycin, Neomycin

A

30S Inhibition

24
Q

Macrolides: Erythromycin, Clarithromycin, Chloramphenicol

A

50S Inhibition

25
Q

Clindamycin

A

More active than tetracyclines –> 50S inhibition

26
Q

Amplicillin, Amoxacillin

A

Cell wall inhibition

27
Q

Quinolones (ciprofloxacin)

A

Inhibition of topoisomerases to interrupt DNA functions

28
Q

Cephalosporins (cephalexin), Bacitracin

A

Cell wall inhibition

29
Q

Sulfamethoxazole/Trimethoprim (Bactrim)

A

Antifolate

30
Q

Metronidazole

A

Reactive intermediate that damages DNA/enzymes

31
Q

Metronidazole

A

Produces reactive intermediate that damage DNA and other sensitive molecules

32
Q

Mupirocin

A

Binds and inhibits tRNA-synthetase for leucine

33
Q

Polymixin B

A

Cationic detergent; interacts as surfactant with negatively charged membrane phospholipids

34
Q

Povidone-Iodine

A

Topical antiseptic/antibacterial

35
Q

Mafenide

A

Acts on G- and G+ bacteria

36
Q

Silver Sulfadiazine

A

Active against bacteria and fungi (burns)

37
Q

Fungi

A

Eukaryotes
Rigid cell walls
Contain ergosterol instead of cholesterol

38
Q

Derm conditions with fungal infections

A

Common members of normal flora
Growth is normally well-constrained
Overgrowth normally only occurs if immune is compromised
- Antibacterial agents do not work against fungi

39
Q

Antifungal Agents

A

Topical: azoles, naftifine, ciclopirox, and the polyene agents amphotericin B and nystatin
Oral: Used for drugs to reach site of infection

40
Q

Griseofulvin

A

Act on microtuble system to disrupt mitosis in certain fungal cells
Not used systemically, common dosing issues, questioning efficacy, + adverse effects and drug interactions

41
Q

Terbinafine

A

PO but 40% loss due to first-pass
Accumulates in skin, nails and fat
Topically too
Inhibits conversion of squalene to alnosterol by squalene epoxidase –> squalene accumulates and ergosterol is decreased
- Rifampin decreases and Cimetidine increases plasma concentration of terbinafine
- ADR with antidepressants, hepatoxicity can occur

42
Q

Azoles- Imidazoles and Triazoles

A

Im: 2 N in 5 membered azole ring - used in OTC/Topical situations
Tri: 3 N in a 5 membered azole ring - used in more serious situations

43
Q

Azole MOA

A

Block fungal P450 dependent synthesis of ergosterol
Disrupts cell membranes –> decrease in ATPase and electron transport enzymes
Inhibits gonadal and adrenal steroids synthesis –> decreases T and cortisol formations
Tri: less effect on human P450 dependent steroid synthetic pathways

44
Q

Itraconazole

A

Potent 3A4 inhibitor

45
Q

Fluconazole

A

Inhibits 3A4 and 2C9 –> raises plasma levels of cyclosporine, phenytoin, tacrolimus, theophylline, warfarin

46
Q

Voriconazole

A

Inhibits 2C19, 2C9, 3A4

47
Q

Posaconazole

A

No CYP inhibition

48
Q

Azole ADR

A

Hepatotoxicity is rare but lead to hepatic failure and deaht
GI distress with nausea, vomiting & diarrhea
Skin irritation, rash, alopecia seen
QT prolongation (except posa)
Visual distrubances and hallucinations (Vor)
NOT IN PREGNANT WOMEN

Integ Exam 1 (7 decks)

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