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Pharmacology Exam 2 > Aminoglycoside Antibiotics > Flashcards

Aminoglycoside Antibiotics Flashcards

1
Q

Aminoglycoside antibiotics core structure made of whaT?

A

1,3 diaminocyclitol linked to one or more aminoglcoside rings

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2
Q

Core structures are what?

A

Streptidine
2-deoxystreptamine
Spectinamine

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3
Q

What do aminoglycosides inhibit

A

Protein biosynthesis

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4
Q

How do amino-glycosides inhibit protein biosynthesis?

A

Binding to 30S ribosomal subunit to the 16S rRNA forming the A site

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5
Q

What step of translation does amino-glycodies interfere with?

A

Formation of initiation complex, causes premature termination

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6
Q

What does aminoglycosides form from its interruption of protein synthesis?

A

Nonsense proteins

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7
Q

Result of formation of nonsense proteins due to aminoglycosdies?

A

Cell wall function impaired

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8
Q

Result of impaired cell wall function in aminoglycosides?

A

More aminoglycosides (AMG) gets in and stops protein synthesis altogether

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9
Q

AMG positively charged or negatively?

A

Positively

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10
Q

What needs to be displaced to get AMG in through outer membrane?

A

Mg++ and Ca++ ions

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11
Q

Why does Mg and Ca need to be displaced?

A

They form salt bridges with phosphates of phospholipids

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12
Q

What type of transport process is passage through cytoplasmic membrane?

A

Active transport

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13
Q

How many bacterial resistance mechanisms have evolved to combat AMG?

A

At least 3

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14
Q

What are the 3 mechanisms that resist AMG?

A

1) Metabolism
2) Altered Ribosomes
3) Altered AMG uptake

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15
Q

How does the metabolism resistance of AMG work?

A

Bacteria inactivate AMG by acetylation, adenylation, and phosphorylation

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16
Q

Are AMGs metabolized by humans or bacteria?

A

Bacteria

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17
Q

How does altered ribosome resistance work?

A

16S rRNA binding site via point mutations

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18
Q

Which bacteria has displayed altered ribosomes in the past?

A

Mycobacterium tuberculosis

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19
Q

How does Altered AMG uptake resistance work?

A

Emergence is far less than resistance due to metabolism

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20
Q

Dangers of AMG?

A

Ototoxic and nephrotoxic

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21
Q

Difference between Ototoxicity and nephrotoxicity in AMG?

A

Ototoxicity is irreversible while nephrotoxicity is reversible

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22
Q

Risk factors for ototoxicity?

A

Using other ototoxic drugs
Reduced renal function
Genetic vulnerability

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23
Q

A less common effect that can result from large doses of AMGs?

A

Curare like effect involving respiratory paralysis

24
Q

How does one deal with the respiratory paralysis caused by AMG?

A

Neostigmine

Calcium gluconate

25
Q

What is the period treatment that AMGs should be discontinued after?

A

5 days

26
Q

Spectrum of antibiotics for AMGs?

A

Gram + and gram -

27
Q

Primary use for AMGs?

A

Gram -

28
Q

What are AMGs usually used in combination with?

A

Penicillin

29
Q

How does AMG and Penicillin combo need to be given?

A

One in each arm to avoid chemical reaction between the two

30
Q

Streptomycin used to treat what?

A

Tuberculosis

31
Q

Most important of the AMGs?

A

Gentamycin

32
Q

Which AMG used for nosocomial infections?

A

Amikacin

33
Q

Streptogramin is a semisynthetic structure derived from what?

A

Pristinamycin 1 and pristinamycin 2 taken from Strep pristinaspiralis

34
Q

Synercid mixture contains what?

A

30% quinupristin

70% Dalfopristin

35
Q

Dalfopristin interfere with protein synthesis how?

A

Interfere with peptide transferase formation of peptide bond between two amino acids

36
Q

How does Quinupristin work?

A

Binds n the ribosomal tunnel and blocks it

37
Q

What provides resistance to Streptogramin?

A

Mutation of A2062 which gates the tunnel exit

38
Q

What is Synercid used IV in treatment of?

A

Vancomycin resistant Enteroccus faecium bacteremia
Skin infection via MRSA
Vanco resistant Enteroccus faecium urinary tract infections

39
Q

Most common resistance to quinupristin due to?

A

Adenine methylation of A2058 in 23S rRNA

40
Q

Streptogramin treatment most likely reserved for what?

A

Life threatening Gram +

41
Q

Senesced use selects for resistant forms of?

A

E. faecialis
E. faecium
S. aureus

42
Q

Toxicity due to synercid?

A

None

43
Q

Does Synercid penetrate blood brain barriers?

A

No

44
Q

Where is concentration of Synercid 50X the extracellular fluid concentration?

A

Macrophage

45
Q

How is Synercid excreted?

A

75% biliary excretion

46
Q

Streptogramins inhibit what enzyme?

A

CYP3A4

47
Q

How does linezolid inhibit protein synthesis?

A

It stops the formation of the 70S initiation complex

48
Q

What is Linezolid used to treat?

A

1) Vanco resistant Enterococcus faecium
2) Nosocomial pneumonia caused by MRSA
3) Skin infections caused by MRSA

49
Q

How is Linezolid taken?

A

Orally or I.V

50
Q

When is linezolid taken?

A

Infections caused by multiple drug resistant Gram +

51
Q

Where has linezolid resistance been reported?

A

Enterococcus species

52
Q

How do organisms develop resistance against linezolid?

A

Target site modification, G to U substitution in peptidyl transferase center

53
Q

What can happen if a patient takes linezolid for more than 6 months?

A

Neuropathy

54
Q

Half life of linezolid?

A

4-6 hour

55
Q

What does Linezolid inhibit non selectively?

A

Monoamine oxidase

56
Q

Lienzolid has potential for interaction with whaT?

A

Adrenergic and serotonergic agents

57
Q

Patients should avoid consuming what when taking Linezolid?

A

Food/beverages rich in tyramine

Pharmacology Exam 2 (9 decks)

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