Pharmacology, Sampson, Block 3, Part 1 Anti-Infective Therapies

Front 1

define selective toxicity

Back 1

capability of antibiotics to kill invading microorganisms without injuring the host

Front 2

3 ways antibiotics utilize selective toxicity

Back 2

- bacteria and prokaryotes = they have a cell wall and mammals do not have a cell wall
- bacterial ribosomes are 70s and human ribosomes are 80s
- bacteria must manufacture folic acid and humans acquire it through diet; folic acid is needed for DNA, RNA, and other protein synthesis

Front 3

define narrow spectrum antibiotic

Back 3

effective only against a few microorganisms ==> always use narrowest spectrum of antibiotic against a microbe

Front 4

define broad spectrum antibiotic

Back 4

effective against huge numbers of bacteria ==> prescribe if known bacterial infection & stop once C&S results are known

Front 5

what is C & S

Back 5

Culture (identifies specific bacteria) & Sensitivity (listing of what antibiotics will kill the organism)

Front 6

define bactericidal antibiotic

Back 6

directly legal to bacteria once significant antibiotic have accumulated

Front 7

define bacteriostatic antibiotic

Back 7

slows microbial growth, but does not cause direct bacterial death ==> meant for person with mature & healthy immune system

Front 8

define minimum inhibitory concentration (MIC)

Back 8

lowest concentration of antibiotic that produces complete incubation of bacterial growth

Front 9

define minimum bactericidal concentration (MBC)

Back 9

lowest concentration of antibiotic that produces 99.9% decline in number of bacterial colonies

Front 10

factors determining duration of antibiotic therapy

Back 10

immunocompromised, elderly, neonate, the infection site (is there a pus pocket blocking?), ID of infecting organism

Front 11

normal duration of antibiotic therapy

Back 11

7 days to "wipe-out" + 3 days to "mop up" infecting bacteria

Front 12

normal duration for your body to produce antibodies

Back 12

7 - 10 days

Front 13

define drug resistant bacteria

Back 13

their growth is not halted by maximum amount of antibiotic that can be tolerated by the host

Front 14

mechanism for bacteria to develop drug resistance

Back 14

Bacterial populations are a heterogeneous mix of sensitive and resistant (generated by spontaneous mutation during replication) bacteria competing for same resources. Sensitive bacteria are killed off first, allowing resistant bacteria to reproduce unchecked.

Front 15

negative outcomes of early discontinuation of antibiotic therapy

Back 15

- treatment failure
- recurrent infection
- drug resistance

Front 16

what is penicillin's distinguishing chemical structure?

Back 16

beta-lactam ring
this group is also called beta-lactam antibiotics

Front 17

compare cell structure of G- and G+ bacteria

Back 17

Both have: inner membrane with PBPs (penicillin binding proteins), peptidoglycan cell wall. G- have an outer membrane with some containing porin channels.

Front 18

how does penicillin work?

Back 18

Bacteria need transpeptidase for cell wall synthesis. Penicillin inhibits PBP which are responsible for transpeptidase synthesis. As a result, cells will go through osmotic lysis. ONLY "baby" bacteria in the process of building cell walls are affected.

Front 19

generally, what is the spectrum of penicillin?

Back 19

- G+ (staph auresum, strep pyogenes, strep pneumoniae)
- G- bacteria with porins (eg Neisseria gonorrhea, Neisseria meningitides),
- Spirochetes (ie Treponema pallidum (syphilis), Borrelia burgdorferi (Lyme disease))

Front 20

describe beta lactamase

Back 20

- bacteria producing enzyme that can dismantle beta-lactam ring of penicillin and cephalosporin molecules, rendering those antibiotics useless
- it is a type of penicillinase

Front 21

list the 4 classifications of PCN

Back 21

- narrow-spectrum penicillinase sensitive
- narrow-spectrum penicillinase resistant (antistaphylococcal)
- broad spectrum (aminopenicillins)
- extended spectrum (anti-pseudomonal penicillins)

Front 22

how are most PCN eliminated?

Back 22

- most are NOT metabolized by liver
- excreted unchanged by kidney; therefore, renal function must be considered

Front 23

what are 3 side effects of PCN?

Back 23

- hypersensitivity (biggest issue), s/s of anaphylaxis are drop BP, can't breath
- GI upset: n/v/d
- Seizure with very high doses

Front 24

what are 2 important PCN drug interactions?

Back 24

- PCN + aminoglycoside in same IV line ==> precipitate
- PCN + probenecid ==> probenecid blocks excretion by kidneys ==> high levels of PCN

Front 25

Penicillin G: what is its classification, how is it administered and why?, how is it eliminated?

Back 25

- Narrow-spectrum beta-lactamase sensitive
- Very unstable at low pH (70% is destroyed by gastric acid); therefore, not given PO
- Excreted unchanged by kidney

Front 26

What do you know about Penicillin V (aka Pen VK)?

Back 26

- Narrow-spectrum beta-lactamase sensitive (like Pen G)
- Better stability in low pH than Pen G
- Can have K+ added for stability, but patients with renal insufficiency are at risk for hyperkalemeia
- Excreted unchanged by kidney

Front 27

What do you know about Depository (aka Depot PCN-G)?

Back 27

- deep IM, z-track injection
- Procain PCN-G lasts 15-24 hours
- Benzathine PCN-G (1-4 weeks)

Front 28

What are two extended spectrum penicillins?

Back 28

- ampicillin
- amoxicillin

Front 29

Compare and contrast two extended spectrum penicillins

Back 29

- Spectrum: G+, enhanced G- (E. coli, P. mirailus, Salmonella, H. flu, Bortadella pertussis, Shigella)
- Need beta-lactamase inhibitor:
- amoxicillin + cluvalanic acid = Augmentin (PO only)
- ampicillin + sulbactam = Unysyn (IV only)
- ampicillin has poor GI absorption, hence IV only
- amoxicillin has better GI absorption and larger spectrum

Front 30

What are 2 reactions of the extended spectrum penicillins?

Back 30

- reduce oral contraceptive effectivity
- persons with mononucleosis will develop a macular rash

Front 31

List 4 antistaphylococcal penicillins (aka narrow spectrum penicillinase resistant)

Back 31

- methicillin (off market now due to almost total resistance)
- oxacillin
- dicloxacilin
- nafcillin

Front 32

How are antistaphylococcals administered and eliminated?

Back 32

- By PO and IV
- Renal excretion except nafcillin, which is bile excretion

Front 33

Describe MRSA

Back 33

- Methicillin Resitant Staph Aureus
- G+, responsible for many skin and superficial structure infections
- Staph Aureus is part of normal skin flora
- nosocomial

Front 34

What is CA-MRSA?

Back 34

- Community Acquired MRSA

Front 35

List 4 antipseudomonal penicillins (aka extended spectrum)

Back 35

- carbenicillin
- mezocillin
- piperacillin
- ticarcillin

Front 36

What is one bacteria that is sensitive to antipseudomonal PCN? Describe it.

Back 36

- Pseudomonas aeruginosa
- G- rod, motile, pili to anchor itself to a cell, common in ICUs
- Causes UTIs, pneumonias, bacterimias, infections in burn and AIDS patients

Front 37

How are antipseudomonal penicillins administered?

Back 37

By IV

Front 38

What are reactions with antipseudomonal penicillins?

Back 38

- They carry high Na+, so be cautious with CHF patients
- Given in same line with aminoglycoside ==> inactivation of aminoglycoside

Front 39

What is etiology of cellulitis?

Back 39

Bacteria (mainly staph aureus) gain access through breaks in the skin and spread rapidly, overwhelming normal body defenses; lesions between the toes from athlete's foot are common entry sites.

Front 40

What is etiology of folliculitis?

Back 40

Same as cellulitis, but bacteria enter through hair follicle causing inflammation of follicle.

Front 41

What is etiology of furuncle (boil)?

Back 41

A tender, dome-shaped skin lesion, typically caused by infection around a hair follicle with Staphylococcus aureus. Can form localized abscesses with pus and necrotic debris at core.

Front 42

What are carbapenems?

Back 42

A drug category "beta-lactam type of ABT"

Front 43

What is the spectrum of carbapenems?

Back 43

Very broad spectrum: good for mixed infections from anaeromes, G+ Staph, G- bacilli, and pseudomonas.

Front 44

Are carbepenems B-lactamase resistant or sensitive?

Back 44

Very b-lactamase resistant

Front 45

Describe the mechanism for imipenem/cilastatin (Primaxin)

Back 45

- Drug category is carbapenems.
- Imipenem weakens bacterial cell wall.
- Cilastain inhibits renal excretion to maintain high levels of ABT

Front 46

How is imipenem/cilastatin (Primaxin) administered?

Back 46

IV, IM only

Front 47

What are the side effects of carbapenems?

Back 47

GI generally, possible hypersensitivity if B-lactam allergic

Front 48

What are cephalosporins and how are they identified?

Back 48

- Drug category: b-lactam
- Identified by generation

Front 49

Rate the generations of cephalosporin in terms of spectrum, beta-lactamase resistance, and distribution to CSF

Back 49

G+ coverage, G- coverage, b-lactamase resistance, dist. to CSF:
1st gen: great, low, low, poor
2nd gen: great, higher, higher, poor
3rd gen: less, higher, higher, good
4th gen: limited, highest, highest, good

Front 50

What are 4 risks with cephalosporins?

Back 50

- allergic rxn, 30% chance of hypersensitivity to cephalosporin if they are allergic to PCN
- notorious for causing C. diff
- bleed risk from a decrease in Vit K (check PT/INR)
- can cause thrombophlebitis (prevention: infuse slowly, rotate IV sites, dilute more drug in NS)

Front 51

Describe pathology of streptococcal pharyngitis (aka strep throat)

Back 51

A common bacterial infection of the throat and tonsils, esp. in children between the ages of 5 and 15, typically characterized by fever, sore throat, painful swallowing, exudates on the tonsils, and swollen anterior cervical lymph nodes. The disease is caused by infection with group A beta-hemolytic streptococci (G+) and may be treated with a variety of antibiotics, including penicillins and macrolides. It may occasionally produce late complications, including rheumatic fever or poststreptococcal glomerulonephritis.

Front 52

Describe Treponema pallidum

Back 52

- a spirochetes (gram negative bacteria that are long, thin, helical and motile)
- causative agent of syphillis
- treatment: benzathine penicillin (narrow spectrum, beta-lactamase sensitive PCN)