Antibodies Flashcards
(64 cards)
1
Q
Selective Toxicity
A
More harm to microbes compared to humans
2
Q
Theraputic Index
A
- Lowest dose to the patient / the theraputic dose
- Increased toxicity lead to topical usage!
3
Q
Theraputic Window
A
Range between Theraputic Dose and Toxic dose
4
Q
Toxic Action
Bacteriostatic
A
- Decreased Growth of bacteria
- still requires immune system to kill
- Example = Sulfa Drugs
5
Q
Bactericidal
A
- Kill or Inhibit Bacteria
6
Q
How is drug –> body spread measured?
A
- Design
- Half-Life
- Appropriate Dosage
- Examples:- Pencilin V = 4/day vs Azitromycin = 1/day
- Kidney/ liver dysfunction if not used properly
7
Q
Spectrum of Activity
Broad-spectrum
A
- wide range of effectiveness
- Positive: can stop acute lif-threatening diseases
- Negative: causes dysbiosis
8
Q
Spectrum of activity
Narrow Spectrum
A
- ID and Susceptibility of pathogen
- Positive: less affect on microbiome
9
Q
Advenrse Side Effects
Types??
A
- Allergic Reactions
- Toxic Effects
- Dysbiosis
10
Q
Adverse Side Effects
Toxic Effects
A
- Resulting from lower TI drugs –> monitoring
- deadly side effects
11
Q
Adverse Side Effects
Dysbiosis
A
- Can result in C. diff growth
12
Q
Resistance by microbes to antibiotics
Types
A
- Intrinisic/ Innate Resistance
- Acquired
13
Q
Resistance by microbes to antibiotics
How is Acquired acquired? 🤣
A
- Mutations
- Horizontal Gene Transfer
14
Q
What antibiotics inhibit cell wal synthesis
A
- Bacitracin
- B-lactam antibiotics
- glycopeptide antibiotics
15
Q
Beta-lactam Antibiotics
What makes it up/ defines it structurally?
A
- Beta-lactam ring
- High TI
16
Q
Beta-lactam Antibiotics
Examples
A
- Carbapenems
- Penicillin
- Cephalosporins
4.Monobactems
17
Q
Beta-lactam Antibiotics
How do they inhibit(esp Penicillin)
A
- Penicillin-Binding Peptides(PBPs) or transpeptidases
- form peptide bridges between adjacent glycanstrands –> less cell wall synthesis
- Only In ACTIVELY GROWING cells!!!
18
Q
Beta-lactam Antibiotics
what weakens/ breaks down these antibiotics
A
- B-lactamase = Penicillinase –> Breaking B-lactam ring
- More powerful version = Extended Spectrum B-lactamases
- CREATED MAINLY BY GRAM (-)!!!
19
Q
Beta-lactam Antibiotics
Penicillin
A
- Extended Spectrum penicillins
- Reduce Gram (+)
- However, can kill Enterobacteriaceae and Pseudomonas
- Affected by B-lactamases
Augmentin = If combined with Beta- lactamase inhibitor, it can counter B-lactamases
20
Q
Beta-lactam Antibiotics
Penicillin G
A
- first natural antibiotic
- Has a high TI
21
Q
Beta-lactam Antibiotics
Cephalosporins
A
- Has a lower PBP affinity with gram(+)
- Has structure which isn’t as affected by B-lactamase
If combined with Beta- lactamase inhibitor, then same logic as penicillin- Later generations(5th) = Effective against MRSA
22
Q
Glycopeptide Antibiotics
How does it work and what does it affect?
A
- Binds to NAM amino acid chain –> No peptidoglycan formation
- Affects Gram(+) bacteria
- Problem: VERY TOXIC
23
Q
Glycopeptide Antibiotics
What are some examples?
A
- Vancomycin
A last resort after Beta-lactam because so toxic and require an IV drip
24
Q
Bacitracin
What are they are how are they used?
A
- Highly Toxic –> Topical Applications
- Peptidoglycan precursor will not transport across the membrane
25
What Antibiotics Inhibit protein synthesis and how do they work?
- Bacteriostatic
- Aminoglycosides are the only bactericidal ones
- Exploit difference between prokaryotic and eukaryotic ribosomes: 70s vs 80s
26
# Aminoglycosides
How do they work?
- Bind to 30s
- They are unable to start translation making it *bactericidal*
- **Cannot be used for anaerobes, enterococci, and streptococci**
```
If penicillin is included, then aminoglycosides can be used
against these things
```
27
# Aminoglycosides
Types/ Examples!
1. Neomycin = Topical usage
2. Streptomycin
3. Gentamicin
4. Amikavicin
5. Tobramycin = Inhaled and can treat Psuedomonas in lungs in Cystic Fibrosis
28
# Tetracyclines and Glycylcylines
What do both do?
- *Reversibly* bind to 30s --> bacteriostatic
- No fRNA attachment --> No translation allowed
- **Equal Gram (+) and Gram (-) atk**
29
# Tetracyclines and Glycylcylines
What are their differences?
- Glycylcylines: wider activity and is good for tetracycline resistant bacteria
30
# Tetracyclines and Glycylcylines
How has there been higher resistance in these?
- Lower Uptake
- Higher Excretion
31
Which antibiotics disrupt cell membrane integrity, and what do they generally do?
- Daptomycin
- Polymyxins
32
# Macrolides
Examples
- Erythromycin
- Azithromycin
33
# Macrolides
What does it do?
- It is used instead of penicilin
- *Reversibly* bind to 50s
- No translation continued
- Bacteriostatic to Gram (+)
--> atypical pneumonia
- **Blocked by Enterobacteriaceae**
34
# Macrolides
How is resistance built?
- Modification of ribosomal RNA Target
- Enzymes causing a chemical modification
- Decreased uptake
35
What inhibit Nucleic Acid synthesis?
- Fluoroquinolones
- Rifamycin's
36
# Chloramphenicol
Actions
- 50s --> No translation
- Wider range
37
# Chloromphenicol
Problem!!
Aplastic Anemia
38
# Fluoroquinolones
What does it do?
- Stops topoisomeraces which stops supercoiling of DNA
- **Bactericidal**
- wider range
- Break DNA gyrase
39
# Fluoroquinolones
How is resistance against built?
Change in DNA gyrase
40
# Rifamycin's
What does it do?
Stops prokaryon RNA polymerase --> No transcription start
- Kills Gram (+), some Gram (-), Mycobacterium
41
# Sulfonamides
What do they do?
- AKA Sulfa Drugs
- Similar to Para-aminobenzoic acid(PABA)
- Chemically bind to enzyme which leads to competitive inhibition
- Work for Gram (+) and (-)
42
# Trimethoprim
What does it do?
- Inhibit enzyme in later step
43
How do Sulfonamides and Trimethoprim work together?
```
co-trimoxazole
```
44
# Daptomycin
What does it do?
- inserts into cytoplasmic membrane
- Used against Gram (+) that are resistant to other antibiotics
45
# Daptomycin
What is resistant to it?
**No Gram (-) because they cannot penetrate the outermembrane**
46
# Polymyxins
What does it do or work with?
- topical usage
- binds to eukaryotic ells
- `works with Daptomycin to bind to Gram (-) membrane`
47
What is Mycobacterium tuberculosis?
- It has a waxy coat
- has less antimicrobial effectiveness
48
# Mycobacterium tuberculosis
What works against it?
- Target cell wall
1. Isoni*azid* = No mycolic *acid* synthesis
2. *E*thambutol = No *e*nzymes --> No synthesis of other cell components
3. *P*yrazinamide = No *p*rotein synthesis
49
# Mycobacterium tuberculosis - Fight!!
What are 1st line drugs
- Have high effectiveness and low toxicity
- `With combination therapy --> resistance can be staved off!`
50
# Mycobacterium tuberculosis - Fight!!
2nd Line
- Used if there is resistance to 1st line drugs
- They are less effective
- They are more toxic
51
# Susceptibility testing
Kirby-Bauer Disc Diffusion Test
- concentration gradient of antibiotic dics to test their power in agar plate with microbe
52
# Susceptibility testing
Zone of Inhibition
Where the antibiotic clears microbe
53
# Susceptibility testing
Minimum Inhibitory Concetraion(MIC)
- Lowest antibiotic concetraion that stops in vitro growth
- Serial dilution
54
# Susceptibility testing
Intermediate
A Microbe with MIC that is between resistant and susceptible
55
# Susceptibility testing
Minimal Bacteria Concentration(MBC)
- Lowest concentration of antibiotic that kills 99.9% of in vitro bacteria killed
- plate count
56
# Susceptibility testing
How is resistance built?
- Misuse of antibiotics
- Cause Increased costs and complications
- Worsens outcomes
57
# Resistance Building
Mechanisms
- Antibiotic inactivating Enzymes
- Alterations in target molecule
- reduced uptake of medicines
- Increased elimination
58
# Resistance Mechanisms
What are the Antibiotic Inactivating Enzymes
- Penicillinase
- Chloramphenicol acetyltransferase
- *Produced Enzymes which interfere with drug*
59
# Resistance Mechanisms
What is altering of target molecule?
- decreased binding of PBPs and ribosomal RNA antibiotics
- Structure changes in molecule --> no binding
60
# Resistance Mechanisms
What is increased elimination defined by?
- **Efflux pumps**
- Remove components of cell by changing pumps
- resistance to range
61
# Resistance Acquisition
(How to stop) Spontaneous Mutation
Can be reduced with more binding sites or combination therapy
62
# Resistance Acquisition
Gene transfer
- can spread resistance to differnt strains, species, and genera
- `can be combined with Spontaneous mutation when R plasmids are transferred`
63
# Preventing Resistance
how is it done?
1. Patient Responsibility
- Follow instructions and dosage taking
2. Educating the Public
- Antibiotics are not used for viruses
- Misuse can lead to problems listed above
64
# Preventing Resistance
How has it become a worldwide problem
1. Animal feed
2. No need for prescripton
3. Overuse
