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Med School > CMOD Exam1 > Flashcards

CMOD Exam1 Flashcards

0
Q

Name three synergistic drug combinations

A
  1. Penicillin + aminoglycosides
  2. Sulfanethoxazole + trimethoprim
  3. Amoxicillin + clavulanic acid
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1
Q

Four main mech of antimicrobials?

A

Inhibition of 1. Cell wall synth

  1. Protein synth
  2. Folic acid biosynthesis
  3. DNA/RNA synthesis
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2
Q

Which drug types are beta-lactams?

A

Penicillins, carbapenems, cephalosporins

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3
Q

What is the MOA for beta-lactams?

A
  1. Binding PBP ( penicillin-binding protein)

2. Destruction of the bacterial cell wall

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4
Q

How do beta-lactams destroy cell walls?

A

Inhibiting transpeptidase, which prevents the cross-linking of peptide glycol molecules in bacterial cell walls.

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5
Q

Which bacteria are beta-lactams most efficient against?

A

Gram positive bacteria, because they have a thick peptidoglycan layer.

Gram negatives are more resistant to beta-lactams bc ther LPS outer layer protects the thin, inner peptidoglycan layer.

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6
Q

Why are beta-lactam inhibitors added to some beta-lactam antibiotics?

A

To overcome resistance by beta-lactamases utilized by some bacteria.

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7
Q

Name two common beta-lactam/beta-lactam inhibitor combinations.

A
  1. Amoxicillin + clavulanic acid

2. Piperacillin + tazobactam

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8
Q

What are the prototypes of penicillins?

A

Penicillin G and penicillin V

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9
Q

Ampicillin: MOA

A

Beta-lactam but increased efficacy against gram-neg bacteria. binds PBPs and inhibits transpeptidase preventing cell wall formation.
Aminopenicillin; the added amino group makes the molecule more hydrophilic and able to cross the lipopolysaccharide layer more easily.

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10
Q

Aztreonam: MOA

A

Bactericidal
Monobactam; preferentially binds PBPs inhibiting cell wall synthesis.

Contains a sulfonic acid group.

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11
Q

Piperacillin: MOA

A

Broad spectrum penicillin; modifications in addition to an aminopenicillin. The extra nitrogen and carbon atoms increase the range of bacteria sensitive to it.

Usually admin in addit to beta-lactamase inhibitor (tazobactam)

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13
Q

Ceftriaxone:MOA

A

“Rocephin”

3rd gen beta-lactam; IV admin; used for STD treatment

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14
Q

Cephalexin: MOA

A

“Keflex”

Cephalosporin; Beta lactam; 1st gen; most common cephalosporin prescribed for outpatient use

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14
Q

Vancomycin: MOA

A

Glycopeptide that binds D-Ala-D-Ala and inhibits the transglycosylase involved in the peptidoglycan synthesis for cell wall.

Affective against Gram positive

Poorly absorbed in GI tract

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15
Q

Vancomycin: MOA+ASX

A

Glycopeptide that binds D-Ala-D-Ala and inhibits the transglycosylase involved in the peptidoglycan synthesis for cell wall.

Affective against Gram positive

Poorly absorbed in GI tract- must be admin via IV

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16
Q

What’s the structural difference between penicillins and cephalosporins?

A

Cephalosporins are more acid stable and made up of a 6 members ring attached to the lactam ring, rather than the thiazolidine ring in penicillins.

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18
Q

How do cephalosporins work?

A

Bactericidal and less susceptible to beta-lactamases. Same mechanism as beta-lactams; irreveribly bind PBPs, preventing them from binding the D-Ala-D-Ala terminus for cell wall synthesis.

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19
Q

Fosfomycin

A

inhibits one of the first steps in the synthesis of peptidoglycan. irreversibly binds enolpyruvyl transferase. Nucleotide precursors accumulate and cell death occurs.

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20
Q

Name the 7 classes of protein synthesis inhibitors

A
  1. aminoglycosides 2. macrolides 3. streptogramins 4. lincosamides 5. oxazolidinones 6. tetracyclines 7. mupirocin
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21
Q

Name an aminoglycoside and give MOA

A

Gentamicin- thought to be bactericidal bc MOA is irreversibly binding 30S ribosomal subunit and also creating fissures and pores in the outer cell membrane.

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22
Q

Whata are the ASX of aminoglycosides?

A

Nephrotoxicity. All aminoglycosides have poor GI absorption and are IV administered. However, they accumulate int eh proximal tubule of the kidney.

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23
Q

Aminoglycosides are particularly affective against….

A

gram-negative bacteria

24
Q

Macrolides: MOA

A

bacteriostatic; bind 23S of 50S ribosomal subunit, inhibiting peptidyl-transferase. This blocks the addition of amino acids to the peptide chain.

25
Q

Name 3 types of macrolides

A

azithromycin, clarithromycin, erythromycin

26
Q

Lincosamides: MOA

A

bacteriostatic; binds 23S of 50S ribosomal subunit, inhibiting peptidyl-transferase. Beneficial in reducing toxin production as well.

27
Q

Example of a lincosamide?

A

clindamycin

28
Q

Tetracycline: MOA

A

bacteriostatic; binds 16S subunit of 30S ribosomal subunit

29
Q

Streptogramins: MOA

A

bacteriostatic; binds 23S of 50S ribosomal subunit interfering with polypeptide chain formation.

30
Q

mupirocin: MOA

A

bactericidal against man gram-positive and gram-negative bacteria. inhibits isoleucyl transfer-RNA synthetase

31
Q

chloramphenicol

A

binds 50S ribosomal subunit near same site as clindamycin and macrolides.

32
Q

Name the 6 categories of drugs that inhibit nucleic acid metabolism or intermediary metabolism

A
  1. fluoroquinolones 2. rifamycins 3. nitroimidazole 4. DHFR inhibitors 5. sulfonamides 6. daptomycin and fidaxomicin
33
Q

Fluoroquinolones: MOA

A

bind and inhibit DNA topoisomerase II in gram-negative bacteria, and inhibits DNA topoisomerase IV in gram-positive bacteria.

34
Q

Rifamycins:MOA

A

binds RNA polymerase and inhibits RNA synthesis.
-highly lipophilic: 1. readily enters mycobacterial cells 2. enters bioflims 3. high CNS distribution 4. enters phagocytic cells, so kills pathogens which are poorly accessible to other drugs.

35
Q

Nitroimidazole- metronidazole : MOA

A

prodrug which is activated in anaerobic bacteria when nitroreductase enzyme (ferredoxin) producing toxic products and free radicals that damage DNA.

36
Q

DHFR inhibitors: MOA

A

combination drug: composed of trimethoprim and sulfamethoxazole. Trimethoprim prevetns converstion of dihydrofolate to tetrahydrofolate, while sulfamethoxazole prevents PABA from being incorporated into folic acid.

37
Q

Daptomycin: MOA

A

bactericial against gram-positive bacteria; bind to cell membrane and cause rapid depolarization, leading to loss of membrane potential and therefore protein, DNA, and RNA synthesis.

inactivated by pulmonary surfactant

38
Q

fidoxamicin

A

“dificid”
inhibits RNA synthesis by inhibiting the sigma-dependent transcription of bacterial RNA polymerases

used against C. diff

39
Q

cotrimoxazole, DHFR inhibitor, has synergistic qualities…how?

A

sulfomethoxazole and trimethoprim are present in a concentration equalling the minimal inhibitory concentrations for each drug independently.

40
Q

amphotericin B: MOA

A

binds ergosterol and causes membrane permeability

41
Q

Azole drugs

A

inhibit 14-alpha-sterol demethylase; inhibits ergosterol synthesis and accumulation os 14-alpha- methylsterols. inhibition of cell membrane.

42
Q

terbinafine

A

inhibits squalene epoxidase, inhibiting ergosterol synthesis (cell membrane). leads to accumulation of squalene, which is toxic to the cell.

43
Q

flucytosine: MOA

A

diffuses into cell wall and is converted into 5-fluorouracil (an anti-cancer drug) which prevents RNA and DNA synthesis

44
Q

caspofungin

A

echocandins; inhibits beta 1-3 glucan synthase, destroys cell wall** (azoles and turbinafine affect cell membrane)

45
Q

flucytosine: ASX

A

gastritis, anemia, leukopenia, (5-fluorouracil affects rapidly proliferating cells)

46
Q

azole: basic MOA

A

inhibits different CYPs (cytochrome P450)

47
Q

which azole cannot penetrate the BBB?

A

ketoconazole

48
Q

which azoles have the worst ASX on GI tract?

A

itraconazole and posaconazole

49
Q

which azoles should not be given to pregnant women and also have the highest solubility?

A

voriconazole and fluconazole

50
Q

Which azole is metabolized by the kidney?

A

fluconazole

51
Q

which azole is used against mucormycosis?

A

posaconazole

52
Q

two topically administered azoles?

A

clostrimazole and miconazole

53
Q

Ciprofloxacin: MOA

A

fluoroquinolone; inhibits topo II- gram neg and topo !V gram positive
antimicrobial

54
Q

Ketoconazole: ASX

A

serious liver damage, adrenal insufficiency, cannot cross BBB, cardia arrhythmogenic events

55
Q

Voriconazole: ASX

A

inhibits widest range of CYPs–> drug-drug interactions, photosensitive dermatitis, elevated liver enzymes, neurologic reactions like hallucinations

56
Q

amphiterocin B: ASX

A

renal toxicity due to ability to cause membrane permeablility, anemia (erythropoetin loss in kidney), abnormal hepatic enzyme levels, seizures

57
Q

Nystatin

A

comparable to amphiterocin B. topical, commonly used for candidiasis

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