Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Class: Immuno Block > Antibiotic_Cell Wall and Mycobacterium > Flashcards

Antibiotic_Cell Wall and Mycobacterium Flashcards

1
Q

Broad Spectrum Antibiotics

A

Drugs that work against both classes of bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Extended Spectrum Antibiotic

A

Drug whose selectivity is broadened by chemical modification.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Gm- outer membrane characteristics. (2)

A

1) Relatively impervious
2) Transport of drugs through TRANSMEMBRANE PORES
a. favor small hydrophilic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What two drugs are too big to be effective against Gm- bacteria?

A

Vancomycin and Daptomycin

- cannot pass through Gm- transmembrane pores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Molecular make up of the Peptidoglycan layer. (2)

A

1) Polysaccharide chain made up of
- N-acetyl-glucosamine (NAG)
- N-acetylmuramic acid (NAM)
2) Five peptide units hanging off of Polysaccharide chain
- Last two peptides are usually D-Ala - D-Ala

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Enzyme that joins the sugars of the polysaccharide chain.

A

Transglycosylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Enzyme that joins the sugar-linked peptides to x-linked polysaccharide chains.

A

Transpeptidase/Penicilin Binding Protein (PBP)/Ser-Enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Penicillin mimics what two AA of the peptide bridge precursor?

A

D-Ala-D-Ala

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Core structure of primary Beta-lactam antibiotics

A

Beta-lactam ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mechanism: Synthesis of peptidoglycan x-link. (2)

A

1) Transpeptidase (Ser-Enzyme) binds D-Ala-D-Ala —> D-Ala-Ser-Enzyme + D-Ala (the last D-Ala got kicked out)
2) Glycine comes in forming a peptidoglycan x-link
a. Ser-enzyme is recycled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mechanism: B-lactam antibiotic action.

A

Penicillin binds Transpeptidase (PBP/Ser-Enzyme)

 - Ser-Enzyme is NOT recycled
 - Bacteria can no longer form Peptidoglycan x-links
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Characteristic: B-lactam antibiotic. (3)

A

1) Irreversible Rxn
2) Effective against GROWING bacteria
3) Bacteriocidal (during peptidoglycan production)
- without peptidoglycan wall, cells burst due to osmotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mechanism and Result: B-lactamase action (3)

A

Hydrolysis of B-lactam ring

1) Serine B-lactamase binds penicillin
2) Forms a complex that allows H2O to hydrolyze B-lactam ring of penicilin
3) A hydrolyzed B-lactam can no longer bind PBP
- Has no therapeutic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Genomic characteristics: B-lactamase (2)

A

Encoded in both chromosomal genes and plasmids

1) Chromosomal B-lactamase genes show INDUCIBLE expression
- Genes are either amplified or expression was upregulated due to environmental changes
2) Plasmid B-lactamase genes are typically expressed constitutively
- Can be transferred from one organism to another
- Responsible for spread of resistance

The genetic origins of B-lactamases will determine whether or not it is effected by B-lactamase inhibitors such as Clavulanic acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

1) Many Cell Wall drugs work selectively against ___
2) Fewer Cell Wall drugs work selectively against ___
Choices: (Gm+ or Gm-)

A

1) Gm+

2) Gm-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clavulanic acid - Most active against:

Detail not important for exam

A

PLASMID encoded B-lactamases

  • Staphylococci
  • Salmonella
  • Shigella
  • H. influenza
  • N. gonorrhoae
  • E. coli
  • K. pneumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Calvulanic acid - Least effective against:

A

Chromosomally encoded B-lactamases

  • Pseudomonas
  • Enterobacter
  • Serratia
  • Citrobacter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Characteristic: B-lactamase inhibitor. (2)

A

Clavulanic acid

1) By itself has NO antibacterial activity
- ONLY effective if combined with other B-lactam antibiotics
2) Bind B-lactamases covalently and inactivate irreversibly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Characteristics: Common Penicilin

A

Penicillin G

1) Acid labile
2) B-lacatamase susceptible
3) Suitable for Gm+, Gm- cocci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Characteristics: Anti-staphlococcal penicillins

A

Cloxacillin

1) Acid STABLE
2) B-lacatamase resistant
3) NOT suitable for:
- enterococci
- anaerobic bacteria
- Gm- cocci
- Gm- rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Characteristics: Extended-spectrum penicillins

A

Amoxicillin

1) Acid STABLE
2) Inactivated by lactamases
3) Greater activity against Gm-
- highly effective in penetrating the outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Uses of Amoxicillin (4)

Not emphasized in lecture

A

1) Sinusitis
2) Otitis
3) UTI
4) Lower respiratory tract infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Adverse reactions: Penicillin (2)

A

1) Superinfection with other microbes
- Oppotunistic microbes such as candidiasis can invade post antibiotic therapy

2) Allergic Reaction
- All penicillins are cross reacting, hence past claims of reactivity are frequently unreliable.

Generally non-toxic at grams/day dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Substitution for patients allergic to Penicillin

A

Cephalosporin (2nd generation or higher)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Resistance: Penicillin (3)

A

1) Upregulation of chromosomally encoded B-lactamases
2) Acquisation of B-lactamases by horizontal gene transfer from other bacteria
3) Mutation of the primary PBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cephalosporin Generations (4)

A

1st: Cefazollin
2nd: Cefamandole
3rd: Ceftazidime
4th: Cefepime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Cephalosporin:

1) Broad spectrum but better for Gm+
2) Restricted to surgical prophylaxis
3) Does NOT penetrate CNS

A

Cefazolin (1st generation Cephalosporin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Cephalosporin:

1) Extended coverage of Gm-
2) No allergic cross-reactivity with penicillin

A

Cefamandole (2nd Generation Cephalosporin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Cephalosporin:

1) Extended gm- activity at the expense of Gm+
2) Effective against inducible B-lactamase but not against constitutive B-lactamase
3) Some cross blood brain barrier

A

Ceftazidime (3rd generation Cephalosporin)

30
Q

Cephalosporin:

1) More resistant to chromosomal B-lactamases
2) True broad spectrum drugs (Both Gm+ and Gm-)
3) Penetrate CNS
4) Appropriate for MRSA

A

Cefepime (4th generation Cephalosporin)

31
Q

Beta lactam cell wall synthesis inhibitors (4)

A

1) Penicillin
2) Cephalosporin
3) Monobactams
4) Carbapenems

32
Q

Newest Cephalosporin approved for use against MRSA.

A

Ceftaroline

33
Q

Characteristics: Monobactams (5)

A

1) Relatively resistant to B-lactamases
2) Active against Gm- rods
3) NO activity toward Gm+
- does not bind transpeptidases of Gm+ or anaerobic bacteria
4) NO cross reactivity with penicillin
5) Given IV

34
Q

Adverse effects: Monobactams

A

No major toxicities. Occasional skin rashs

35
Q

Characteristic: Carbapenems (5)

A

1) Broad Spectrum
2) There may be CROSS-SENSITIVITY in patients with penicillin allergies
3) Penetrate CNS
4) All cleared renally
5) Given IV
6) Resistant against serine B-lactamases but not metallo B-lactamases

36
Q

Given with some carbapenems to inhibit renal dehydropeptidases. (Increase half life of carbapenems)

A

Cilastatin

37
Q

Carbapenem drug resistant to modification by renal dehydropeptidases

A

Meropenem

38
Q

Monobactam drugs

A

Aztreonam

39
Q

Carbapenem drugs (2)

A

1) Imipenem

2) Meropenem

40
Q

Adverse effects: Carbapenems (2)

A

1) Nausea, vomiting, diarrhea, skin rashes.

2) Seizures may occur in patients with renal insufficiency

41
Q

Non-B-lactam cell wall synthesis inhibitors

A

1) Vancomycin

42
Q

1) Glycopeptide
2) Active against Gm+, esp. staphlyococci
3) Bactericidal for actively growing cellls
4) Binds the cell wall rather than enzymes used to make it
5) Enter CNS

A

Vancomycin (IV)

43
Q

Antibiotics: Glycopeptides

A

1) Vancomycin
2) Oritavancin
3) Dalbavancin

44
Q

Mechanism: Vancomycin (2)

A

1) Drug binds tightly to D-Ala-D-Ala

2) Binding interferes with BOTH transglycosylation and transpeptidation reactions

45
Q

Resistance: Vancomycin

A

1) Switch in the peptidoglycan pentapeptide from D-Ala-D-Ala to D-Ala-D-Lac (Lactic acid)
- Leads to a loss of hydrogen bond that decreases affinity of drug to pentapeptide by 1000 fold

46
Q

Adverse effects: Vancomycin (3)

A

Minor:

1) phlebitis at injection site
2) chills, fever
3) rare ototoxicity and nephrotoxicity

47
Q

Important Drug Combination: Vancomycin

A

Often given with aminoglycosides or gentamicin for treatment of enterococcal infections

48
Q

Alternative drugs to Vancomycin due to Vancomycin’s long term IV use. (7-10 days of IV injection at hospital required for treatment) (2)

A

1) Dalbavancin
- Administered in two injections.
- First injection - Day one
- Second injection - Day eight

2) Oritavancin
- Only need ONE IV dosing

49
Q

Antibiotics: Lipopeptides (2)

A

1) Daptomycin (Pore former)

2) Polymyxin (Membrane disrupter)

50
Q

Antibiotic:

1) Forms pores in membrane that allow K+ loss without cell rupture
2) There is NO release of toxins
3) Approved for Gm+ skin and soft tissue infections that involve MRSA
4) 7-14 days by IV

A

Daptomycin (Lipopeptide)

51
Q

Antibiotics:

1) Bind outer membrane of Gm- leading to permeability of both inner and outer membranes
2) Commonly used topically in form of triple antibiotic (neosporin)

A

Polymyxins (Lipopeptide)

52
Q

Antibiotic:

Inhibit MurA - preventing conversion of NAG to NAM

A

Fosfomycin

53
Q

Characteristics: Fosfomycin
Resistance:
Utility:
Pregnancy usage:

A 
Resistance - Loss of drug transport into cell
   - MurA of TB is naturally resistant
Utility - Active against Gm+ and Gm-
   - Used for uncomplicated UTIs
Pregnancy - Oral administration only
54
Q

Antibiotic:

Inhibit lipid phosphatase that dephosphorylates lipid carrier of peptioglycan subunits

A

Bacitracin

Peptidoglycan mechanism:

1) NAM-NAG-pentapetide complex is assembled inside the cell
2) Complex attaches to a phopholipid facing the inside of the cell
3) In order for the phopholipid to attach to the NAM-NAG complex, it must first get dephosphorylated
4) Bacitracin inhibits the dephosphorylation of the phospholipid preventing it from attaching to the NAM-NAG complex

55
Q

Characteristics: Bacitracin (3)

A

1) ONLY active against Gm +
2) Only used topically because of nephrotoxicity
3) Usually used in combination with other antibiotics

56
Q

Antibiotic:

Competitive inhibitor of Alanine racemase and D-Alanine ligase

A

D-Cycloserine

D-Ala-D-Ala synthesis

1) L-Ala inside the bacterial cytosol is converted to D-Ala by Alanine Racemase
2) Two D-Ala are put together by D-alanine ligase

57
Q

Characteristics: D-cycloserine

A

1) Structurally related to D-alanine
2) Drug is reserved for TB treatment
- Second line drug with serious side effects:
- Dose related CNS toxicity

58
Q

Drugs that target Mycolic Acid. (3)

A

1) INH
2) ETA
3) PAS

59
Q

1st line prodrugs for TB: Activation by bacteria is required. (2)

A

1) PZA –> POA (Pyrazinoic Acid)

2) INH –> INH-NAD

60
Q

1) Targets large beta subunit of RNA Polymerase - inhibiting elongation
2) Effective against slow growing INTRACELLULAR Mtb

A

Rifampin (RIF)

61
Q

Target Mycolic acid

A

Isoniazid (INH)

62
Q

Inhibits protein synthesis in DORMANT bacteria

A

Pyrazinamide (PZA)

63
Q

1) Target Arabinogalactan

2) Effective against fast growing EXTRACELLULAR Mtb

A

Ethambutol (EMB)

64
Q

Bacterial enzyme that activates prodrug INH –> INH-NAD

A

KatG (Catalase Peroxidase)

65
Q

Target of INH-NAD

A

Fab1 (InhA) of FAS-II

- Prevent elongation of Mycolic acid

66
Q

Vitamin responsible for adverse effects of INH

A

Pyridoxine (B6)

67
Q

What mechanism effects INH metabolism

A

Acetylation

68
Q

Effect of Rifampin on excreted body fluids.

A

Turns urine, sweat, and tears purple and red.

Benign

69
Q

Advantages of Rifabutin and Rifapentine over Rifampin (RIF) (4)

A

1) Longer half life
2) More Potent
3) Better membrane permeability - enter macrophages easier
4) Decreased induction of CYP3A - allows better compatibilty with other medications

70
Q

POA mechanism

A

1) Inhibit RpsA from binding tmRNA

2) Inhibit Trans-Translation

71
Q

Adverse Effects: EMB

A

Red-Green color blindness and Optic Neuritis

- Hence, NOT prescribed to children

Class: Immuno Block (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions