Antiinfective therapy + Beta lactam Flashcards

1
Q

Gram Pos mnemonic

A

gram Pos–Purple–^Peptidoglican–Penicillin

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2
Q

Gram Neg mnemonic

A

gram Neg–Not Nice polysacaride–eNdotoxin

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3
Q

How to differentiate staph and strep (2)

A

Staph: catalase + , grape clusters
Strep: catalase -, diplococci/chains

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4
Q

Gram-neg pathologic think

A

Aerobic bacilli

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5
Q

Anerobic think

A

deep abscess (ie bacteroides)

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6
Q

Glucose fermenters think

A

like the gut (Enterobacteriaceae)

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7
Q

3 categories of anti-infectives: PED

A
  1. Prophylactic therapy: prevent infection
  2. Empiric therapy: treat suspectd infect’n–towd “most likely”
  3. Definitive therapy: treat known infective agent-culture-> sensitivity
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8
Q

Teenager CAP, pathogen and treatment

A
  • Mycoplasma,

- macrolide –> azithromycin

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9
Q

Antiinfective MO’s (5)

A
  1. inhibition of Cell Wall synthesis
  2. protein synthesis inhibitors
  3. Inhibition of nucleic acid replication and transcription
  4. Inhibition of synthesis of essential metabolites
  5. Plasma membrane injury
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10
Q

Cell Wall synthesis inhibitors (4)

A
  1. penicillin
  2. vancomycin
  3. cephalosporins
  4. bacitracin
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11
Q

Protein synthesis inhibitors (4) (bacteriostatic)

A
  1. Chloramphenicol
  2. erythromycin
  3. tetracyclines
  4. streptomycin
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12
Q

Nucleic acid replication inhibitors (2) (bacteriocidal)

A
  1. Quinolones

2. rifampin

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13
Q

Essential metabolite synthesis inhibitors (2)

A
  1. Sulfanilamide

2. Trimethoprim

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14
Q

Plasma membrane injury (1) (topical)

A
  1. Polymyxin B
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15
Q

fungi version of cholesterol in cell wall–helps hold wall together

A

ergosterol

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16
Q

spectrum of activity can be _______ or _______

A

wide or narrow

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17
Q

anaphylaxis and hives are:

A

Type I hypersensitivity rxn

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18
Q

Ways toxicity can happen: (3)

A
  1. extension of mehanism of action
  2. Unintended physiologic interaction
  3. Dose-related
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19
Q

an infection that occurs during or after treatment of another pre-existing infection–may result from the treatment itself or changes in I.S

A

secondary infection

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20
Q

a new infeciton occuring in a pt having a preexisting infection

A

Superinfection

21
Q

Bacteria can resist action of antibiotics by: (4)

societal vs. patient level

A
  1. preventing access to target of antibiotic
  2. degrading antibiotic
  3. altering antibiotic
  4. rapid extrusion of antibiotic
22
Q

DDDD for antibiotic resistance

A
  1. Disable – inactivation of the antibiotic (usually by a beta-lactamase
  2. Disguise – modification of target proteins (MRSA)
  3. Deter – impaired entry of antibiotic into bacteria
  4. Discharge – ejection of antibiotic by EFFLUX PUMPS
23
Q

Guidelines for antiinfection use: study pg 15

Imp for Sanford Guide

A
  1. Don’t use antibiotic for COLONIZATION/ CONTAMINATION
  2. Use most narrow-spectrum agent appropriate for pt infection
  3. Use proper does
  4. Use shortest effective during of therapy
24
Q

cell wall inhibitor–prevent cross-linking

A

beta-latam inhibitor–bactericidal by intervering w/ the trnaspeptidation rxn of bacterial cell wall synthesis

25
Q

almost all beta-lactam’s end in ______ or ______ or start with______

A

-cillin (PCNs),
-penem
ceph-

26
Q

Mechanisms of beta-lactam antibiotic drug resistance (2)

A
  1. inactivation of antibiotic by beta-lactame

2. modification of PBPs (penicillin binding protein)

27
Q

beta-lactames won’t treat

A

MRSA–resistant to all 3 types of penicillins

will treat MSSA (methisilin sensitive Staph aureus)

28
Q

beta-lactames excreted in active form in urine, so we should think…

A
  1. dose adjustmetns needed w/ renal impairments

2. can be used to treat UTI’s

29
Q

penicillin classes

A
  1. natural penicillin (form directly form mold ex. PCN G & V)
  2. antistaph penicillins
  3. extended-spectrum penicillins
30
Q

penicillin have _____ protein binding, doesn’t like to go into _____

A

high–,

CSF–w/ meningitis BBB not as function—> penicilin

31
Q

Penicillin V (oral vs. parenteral G) _________ activity against Gram+ orgs, Gram - cocci, and non-beta lactamase producing anaerobes

A

GREATEST – resistance high though

32
Q

Penicillin V have ______ activity agains Gram- _____

A

little,

rods

33
Q

Penicillin V K (oral) (potassium pairing for less acid inactivation) indicated for

A

mild to moderate infections (strep throat, otitis media, impetigo)–because v bioavailablity

34
Q

Penicillin V can be given with meals but _______ is _______ if given on an empty stomach

A

absorption is improved

35
Q

Penicillin V ADR’s (3)

A
  1. GI disturbances
  2. Hypersensitivity (allergy)
  3. Secondary infection
36
Q

anti staff penicillin

A

methicillin

37
Q

Main Gram+ w/ more Gram- coverage

A

Aminopenicillins (Extended-spectrum penicillins)

38
Q

better at crossing porin channel

A

Amoxicillin

39
Q

Good for ENT infections, GU, skin/skin structure infections, pneumonia, part of triple therapy for H. pylori

A

Amoxicillin–great against Streptococcal species

40
Q

Use amoxicillin ______ and ampicillin_______

A

orally,

parenterally

41
Q

Augmentin

A

Amoxicillin w/ Clavulanate ( Beta-lactmase inhibitor)

42
Q

Amoxicillin + clavulante potassium

A

Augmentin–take at start of meal

43
Q

Cephalosporins–generations?

A
1st  -- good for Gram+
2nd
3rd
4th -- best for Gram-
5th -- best for Gram+
44
Q

Cephalosporins mode of action

A

same as other beta-lactams–not good on MRSA–bad on pseudomonas

45
Q

Fifth generation Cephalosporin targets

A

MRSA–penetrates CNS plus 4th

46
Q

VRE

A

vancomycin resistant enterococcus

47
Q

Impetigo:
Group A strep:
Staph. Aureus:

A
  • “honey crusted” lesions (non-bullous)

- Bullous

48
Q

similar to other beta-lactam antibiotics – no cross-resistance btwn penicillins

A

Carbapenems (popular: imipenem) – hospitals and ICUs–LIVER TOXIC

49
Q

new synthetic class of moncyclic beta- lactam–narrow spectrum–ONLY binds to PBP in Gram-neg aerobic bac

A

Monobactams–look at end of beta-lactan ppt for summarys!!!