Antibiotics (Exam V) Flashcards

1
Q

What color do gram + bacteria stain with? Why is this?

A
  • Purple-Blue (Techoic acid stains to the peptidoglycan)
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2
Q

What makes up the cell wall in bacteria?
In which bacteria is this cell wall much bigger?

A
  • Peptidoglycan
  • Gram+ bacteria
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3
Q

What color do gram - bacteria stain with?
What characteristics do gram- bacteria have?

A
  • Reddish-orange
  • Second outer membrane on top of a thinner cell wall
  • Gram - bacteria have lipopolysaccharides in their outer membrane.
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4
Q

What occurs if too many gram - bacteria are killed off too quickly?
Why is this?

A
  • Endotoxic Shock Syndrome
  • Massive release of lipopolysaccharides that are converted into endotoxin.
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5
Q

What shape do gram + bacteria often have?
What about gram - bacteria?

A
  • Gram + = spherical (cocci)
  • Gram - = rods (everything else)
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6
Q

Differentiate bactericidal & bacteriostatic.

A

Bactericidal = kills bacteria
Bacteriostatic = prevents replication/growth

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7
Q

What is the most broad spectrum antibiotic class?
Why are these safer for humans?

A
  • Ribosome Protein Synthesis Inhibitors
  • Inhibit ribosomes 50S & 30S that humans don’t have.
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8
Q

What types of ribosomes do bacteria have?

A
  • 50S & 30S (& 70S)
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9
Q

What types of ribosomes do humans have?

A
  • 40S, 60S, & 80S
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10
Q

What structure is highlighted in red below?

A

β-lactam ring

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11
Q

How do β-lactam containing ABX’s inhibit cell wall synthesis?

A
  • The β-lactam ring binds & blocks the enzymes that cross link the peptidoglycans that form the wall.
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12
Q

What drug is indicated by 1 on the figure below?

A

Penicillin

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13
Q

What drug is indicated by 2 on the figure below?

A

Cephalosporin

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14
Q

What type of bacteria do cell wall inhibitors work best on?

A

Gram +

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15
Q

What type of bacteria do cell membrane disruptors work best on?

A

Gram -

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16
Q

What is the most common drug allergy that exists?

A
  • Penicillin allergy (urticaria, redness, etc.)
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17
Q

What are carbapenems useful for?
What are they the drug of choice for?

A
  • β-lactamase bacteria & when CNS penetration is needed.
  • Enterobacter (drug of choice)
18
Q

What drug is good for penicillin resistant gram + bacteria (MRSA)?
How does it work?

A
  • Vancomycin
  • Binds to amino acids & prevents cross-linking of peptidoglycans.
19
Q

What adverse reactions can occur from vancomycin?

A
  • “Red-neck” Syndrome - neck flushing from histamine release
  • Ototoxicity
  • Nephrotoxicity
  • Chills/fever
20
Q

How do cell membrane disruptors work?

A
  • Act as detergents essentially. Bind to phospholipids in membrane & create pores.
21
Q

Can Polymixin be used systemically to treat infections? Why or why not?

A
  • Last resort for resistant gram - strains
  • Very neuro & nephro toxic
22
Q

What drug classes are protein synthesis inhibitors?

A
  • Tetracyclines
  • Macrolides
  • Aminoglycosides
  • etc.
23
Q

What kind of structure do tetracyclines have?
Are they bacteriostatic or bactericidal?

A
  • 4-ring structure
  • Bacteriostatic
24
Q

What is the biggest side effect of tetracyclines when used with adults?
Why is this?

A
  • N/V/D & gastric upset.
  • Very broad spectrum & can destroy normal intestinal microbiota
25
Q

Why are tetracyclines not given to children?

A
  • Abnormal bone development
26
Q

Name the two macrolides discussed in lecture. What advantage does one have over the other?

A
  • Erythromycin
  • Azithromycin (short course, 4-5 days)
27
Q

What drug, discussed in lecture, binds to bacterial RNA polymerase?

A
  • Rifamycin
28
Q

How do Fluoroquinolones work?
What characteristics do these drugs have?

A
  • Inhibition of DNA gyrase
  • Excellent gram - activity
  • Good gram + activity
29
Q

Which drugs are bacterial DNA/RNA synthesis inhibitors?

A
  • Rifamycin
  • Fluoroquinolones (Cipro, Levaquin, & floxins)
30
Q

Which drugs are inhibitors of folic acid synthesis?

A
  • Sulfonamides
  • Trimethoprim
31
Q

What is the mechanism of action of bacterial folic acid synthesis inhibitors?

A
  • Prevent conversion of PABA into DHF (dihydrofolic acid) → → folic acid.
32
Q

What are sulfonamides often used for?
What are they often used with?

A
  • Pneumocystitis & toxoplasmosis
  • Often paired with Trimethoprim
33
Q

What antifungals need to be known?

A
  • Imidazole
  • Amphotericin
  • Lamisil
34
Q

What three antiprotozoan agents need to be known?

A
  • Quinine
  • Hydroxychloroquine
  • Metronidazole (Flagyl)
35
Q

What is metronidazole used for?

A

Giardia & trichomoniasis

36
Q

What are the side effects of metronidazole?

A
  • Black “hairy” tongue (can last a year)
  • Birth defects
  • Cancer
37
Q

What drug is used to treat river blindness roundworm?

A
  • Ivermectin
38
Q

How does bacterial antibiotic resistance develop?
Describe extrachromosomal mutation.

A
  • Chromosomal mutation
  • Extrachromosomal mutation (f-plasmid forms f-pilli with another bacteria thus transferring its resistance.
39
Q

How does premature termination of antibiotics propagate antibiotic resistance?

A
  • Highly resistant bacteria take longer to be killed by antibiotic so if stopped early then the highly resistant ones are the only ones left that can reproduce.
40
Q

What can be used for a horrible C-diff infection to restore normal intestinal flora?

A
  • Fecal Transplant.