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PDA 3 > Gulsevin Exam 2 Materials > Flashcards

Gulsevin Exam 2 Materials Flashcards

1
Q

Aminoglycosides

Are aminoglycosides acidic or basic?

A

basic, postively charged

especially at low pH, readily water soluble, poor absorption in GI tract

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2
Q

Aminoglycosides

How do Aminoglycosides enter the cell of the target organism?

A
  • passive infusion through porins
  • passage through membrane disruption

outer membrane, (-) charge interacts with drug, (+) charge

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3
Q

Aminoglycosides

How do Aminoglycosides enter the cytoplasm of the target organism?

A
  • Proton motive force drives drug entry into the cytoplasm (H+ pumped out, drug (+ charged) pumped in)
  • Oxygen-dependent process involving protein pumps

highly acidic enviroment or lack of oxygen= interfers with drug entry

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4
Q

Aminoglycosides

What is the mechanism of action of Aminoglycosides?

A
  1. blocks initiation of protein synthesis
  2. blocks further translation and elicits premature termination of protein synthesis
  3. incorporation of incorrect amino acid of protein synthesis

bacterialcidal, because bacteria cannot make essential proteins

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5
Q

Aminoglycosides

What is the binding site of aminoglycosides?

A

A-site of the ribosomal subunit

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6
Q

Aminoglycosides

What are the metabolism mechanisms of resistance to aminoglycosides?

A
  • aminoglycoside acetylases (AAC)
  • aminoglycoside phosphorylases (APH)
  • aminoglycoside nucleotide transferases (ANT)

sites on the structure can be modified to avoid resistance

overall, resistance mechanisms include: metabolism, prevention of drug entry, mutation of drug target site

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7
Q

Aminoglycosides

What are the entry preventions mechanisms of resistance to aminoglycosides?

A
  • mutations of the porin genes or lower porin expression may prevent drug entry into cells
  • changes to membrane chemistry (change in charge) and composition can prevent effective contacts between aminoglycosides and the membrane surface
  • changes that affect the proton motive force can decrease the aminoglycoside intake
  • efflux pump overexpression can result in increased removal of aminoglycoside from the cell

overall, resistance mechanisms include: metabolism, prevention of drug entry, mutation of drug target site

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8
Q

Aminoglycosides

What are the drug target site mechanisms of resistance to aminoglycosides?

A
  • single nucleotide mutations near the A site of the 16S rRNA can result in diminished binding
  • methylation of the 16S rRNA mediated by methyltransferases can modify specific nucleotides preventing binding
  • mutations in ribosomal proteins may prevent binding
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9
Q

Aminoglycosides

What is the use of replacing one of the sugar molecules of the aminoglycoside structure with a 5-membered ring?

A

extended spectrum to gram (+)

BUT it is more susceptible to degradation

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10
Q

Aminoglycosides

What aminoglycoside is used for the treatment of hepatic encephalopathy?

A

Neomycin B

MOA: supress bacteria in gut that produce urease (urea -> CO2 + NH4+)

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11
Q

Aminoglycosides

What are the adverse effects of Aminoglycosides?

A
  • OTOTOXICITY, damage to the structures of the inner ear can lead to hearing loss, tinnitus, and/or balance disturbances. typically IRREVERSIBLE and can occur at therapeutic doses
  • NEPHROTOXICITY, high quanities excreted in the urine, therefor kidney disfunction may require a reduced dose to prevent accumulation to toxic levels. increase risk of ototoxicity
  • NEUROMUSCULAR JUNCTION BLOCKADE (less common) and may exaggerate muscle weakness in patients with myasthenia gravis or parkinsonism
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12
Q

Aminoglycosides

What drug class cannot be given with aminoglycosides in the same solution of at the same administration site?

A

beta-lactams

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13
Q

Macrolides

What is the binding site of Macrolides?

A

23S of ribosomal subunit

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14
Q

Macrolides

What is the mechanism of action of macrolides?

A

binds 23S rRNA to prevent further elongation of protein chains

bacteriostatic

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15
Q

Macrolides

How is Erythromycin formulated for IV delievery?

A

salf formation with acids (increased H2O solubility)

erythromycin is not very water soluble as free base

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16
Q

Macrolides

What is the half-life of Erythromycin?

A

1.5-2 hours, requires 4x/day dosing

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17
Q

Macrolides

What can be done with the formulation of Erythromycin to assist with it’s unpleasant taste?

A

prodrug formulation
- erthromycin ethylsuccinate (oral tablet and granules for oral suspension)
- stearate salt
- enteric coated

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18
Q

Macrolides

What is the route of metabolism of Erythromycin?

A

extensive metabolism via CYP3A4 in the liver, 80% is inactivated through demethylation, ~60% is excreted in the bile

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19
Q

Macrolides

How can Erythromycin be degradated after administration?

A
  • gastric acidic enviroment
  • self- degradation
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20
Q

Macrolides

What is the importance of structural changes in Clarithromycin and Azithromycin compared to Erythromycin?

A
  • acid stability
  • circumvent ketal formation (self-degradation)
    overall, increased oral absorption and improved half life

also have a broader spectrum of action

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21
Q

Macrolides

What are the indications of Clarithromycin?

A
  1. Mycobacterium avium complex (MAC) in patient with AIDS
  2. H. pylori associated with duodenal ulcers
  3. Community-acquired pneumonia
  4. Sinusitis
  5. Acute exacerbations of chronic bronchitis

penetrates lung tissue and macrophages better than erythromycin

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22
Q

Macrolides

What is the dosing regimen of Clarithromycin?

A

2x/day dosing

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23
Q

Macrolides

What is the dosing of Azithromycin?

A

once daily dosing

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24
Q

Macrolides

What are the indications of Azithromycin?

A
  1. Mycobacterium avium complex (MAC) in patient with AIDS
  2. Otitis media
  3. Community-acquired pneumonia
  4. Sinusitis
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25
Q

Macrolides

What are the adverse effects of Macrolides?

A

GI upset (severe with erythromycin, mild with other macrolides)

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26
Q

Macrolides

What macrolid inhibits CYP3A4?

A

-erythromycin
-clarithromycin

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27
Q

Macrolides

What are the mechanisms of resistance to macrolides?

A
  • N6 dimethylation
  • mutations which change nucleotide identity
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28
Q

Tetracyclines

Are tetracyclines acidic or basic?

A

basic

typically protonated (+) under physiological conditions

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29
Q

Tetracyclines

What is the mechanism of action of tetracyclines?

A

bind to the 30S subunit= block tRNA binding to A site= inhibition of protein synthesis

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30
Q

Tetracyclines

What are the uses of tetracyclines?

A

ATYPICAL infections, GRAM (+), and GRAM (-)
- tick borne illnesses (Babesiosis, Lyme Disease, Anaplasmosis, Tularemia, Ehrlichiosis, Rocky Mountian Spotted Fever)
- Rickettsial infections
- STIs (chlamydia, gonorrhea, syphilis)
- Malaria
- Bacillius anthracis (Anthrax)
- doxycycline & minocycline= acne vulgaris and rosacea

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31
Q

Tetracyclines

What are the adverse drug interactions of tetracyclines?

A

METALS
avoid metal supplements including iron, magnesium, calcium, zinc, and antacids

tetracyclines chelates metal ions= decreased absorption

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32
Q

Tetracyclines

What structural modification leads to tetracyclines to be unstable in acidic and basic conditions?

A

hydroxyl group at C6

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33
Q

Tetracyclines

What are the adverse effects of tetracyclines?

A

Fanconi syndrome

due to metabolite, epianhydrotetracycline

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34
Q

Tetracyclines

What are the mechanisms of resistance to tetracyclines?

A
  • mutations of efflux pumps (tetracycline resistance genes tetA, tetB, tetC)
  • ribosomes protection proteins (Tet(M), Tet(O))
  • enzymatic degradation of tetracycline through the tetX protein
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35
Q

Fluroroquinolones

Are fluroquinolones bactericidal or bacteristatic?

A

bactericidal

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36
Q

Fluoroquinolones

Why are fluoroquinoles a preferred treatment?

A

high bioavaliability and wide spectrum of action

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37
Q

Fluroquinolones

What is the spectrum of action of Nalixidic acid?

A

most gram negative

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38
Q

Fluoroquinolones

What is the mechanism of gyrase?

A
  1. DNA gyrase binds to 2 segments of DNA, creating a node of positive superhelix
  2. The enzyme then introduces a double strand break in the DNA and passes the front segment through the break
  3. The break is then resealed creating a negative supercoil
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39
Q

Fluroquinolones

What is the mechanism of action of Fluroquinolones?

A

stabilizes DNA to prevent the step necessary to supercoiling

variations in fluro structures leads to variation in DNA intercalation

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40
Q

Fluroquinolones

What are the interactions of Ciprofloxacin at the binding site, S. aureus gyrase?

A
  • pi-pi binding
  • hydrophobic interactions
  • hydrogen bonding
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41
Q

Fluroquinolones

What is the purpose of modifying fluroquinolone drug structure?

A
  • increase the drug potency
  • altering the selectivity profile
  • reduce drug metabolism
  • increase the drug bioavaliability

modification made @ N-1, C-7, and some C-3

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42
Q

Fluroquinolones

What is the optimized modification at N-1 on Fluroquinolones?

A

4>5 carbon chain off of N-1 capped with an amine

effects are length dependent, not too short or too long

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43
Q

Fluroquinolones

What are the possible modifications at the C-3 position?

A

ester groups instead of acid may be utilized because they have better cell penetration and can be prodrugs

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44
Q

Fluroquinolones

What is the purpose of modifying the C-7 site on fluroquinolones?

A

changes to the C-7 site can change the drugs selectivity
large, extended, bulky groups have diminished activity

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45
Q

Fluroquinolones

What is the therapeutic effects of substituting a piperazine ring analogue at C-7?

A

more effective against gram (-) and pseudomonas

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46
Q

Fluroquinolones

What is the therapeutic effects of substituting a pyrrolidine ring analogue at C-7?

A

more effective against gram (+), atypical organisms, respiratory organisms, and streptococcus pneumoniae

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47
Q

Fluroquinolones

What are the adverse drug interactions of fluroquinolones?

A

METAL
avoid metal supplements like iron, calcium, zinc

fluroquinolones chelates metal ions= decreased solubility

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48
Q

Fluroquinolones

What Fluroquinolones are redily found in the urine making them good UTI drugs?

A

Ciprofloxacin (45% recovered in urine) and Levofloxacin (87% recovered in urine)

Moxifloxacin 20% in urine and Gemifloxacin ~36% in urine

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49
Q

Fluroquinolones

What are the adverse effects of Fluroquinolones?

A
  • tendinitis and tendon rupture
  • CNS effects
  • phototoxicity/photosensitivity
  • arthropathy (joint diseases)
  • QT prolongation
  • retinal detachment
  • peripheral neuropathy
  • GI effects
  • hyper/hypoglycemia
50
Q

Fluroquinolone

What Fluroquinolone has the highest risk of QT prolongation?

A

Moxifloxacin

51
Q

Fluroquinolones

What are the mechanisms of resistance to Fluroquinolones?

A
  • mutations of gyrase can prevent binding
  • increase expression of efflux pumps
  • if fluroquinolone has a piperazine ring at C-7 then it can be acetylated via mutant aminoglycoside-modifying enzyme

ciprofloxacin contains piperazine ring and can be metabolized

52
Q

Fluroquinolones

Why do Fluroquinolones have an enviromental impact?

A

since they are renally excreted mostly unchanged they can enter the sewer system

53
Q

Bacitracin

What organisms is Bacitracin effective against?

A

gram (+)

54
Q

Bacitracin

What is the main use of Bacitracin?

A

topical treatment of minor skin injuries

55
Q

Bacitracin

What are the adverse effects of Bacitracin?

A

allergic reaction (fever, hives, itching, swelling of lips and face, difficulty breathing, nausea, vomiting)

56
Q

Bacitracin

What is the pregnancy risk category of Bacitracin?

A

C

no evidence of risk of fetal harm with use of topical bacitracin

57
Q

Polymyxins

What is the use of Polymyxins?

A
  • systemic infections caused by multi-drug resistant gram (-) bacteria, including: Enterobacteriaceae, Pseudomonas, Acinetobacter
  • topically for otitis externa and bacterial conjunctivitis
  • may be used IM or IV in sulfate salt formulation to treat serious UTI, meningitis, or septicemia

not first line

58
Q

Polymyxin

What is the mechanism of action of Polymyxin?

A

polymyxin binds to the bacterial membrane with the lipids (LPS and Lipid A) which results in the displacement of Ca2+ and Mg2+ ions= disruption in the membrane structure, increased permeability, and subsequent rupture

59
Q

Polymixins

What are the adverse effects Polymyxins?

A
  • nephrotoxicity (hemauria, oliguria, and acute renal failure)
  • neurotoxicity
  • neuromuscular blockade

side effects limit use to multidrug-resistant infections-not first line

60
Q

Vancomycin

What are the uses of Vancomycin?

A

GRAM POSITIVE ONLY
- methicillin-resistant staphlocococcus aureus (MRSA)
- C. difficile
- Enterocolitis caused by S. aureus

61
Q

Vancomycin

Why must Vancomycin be given via IV?

A

poor oral bioavaliability

oral form is for C. diff only

62
Q

Vancomycin

What is the mechanism of action of Vancomycin?

glycoprotein

A

inhibits PGT preventing synthesis of peptidoglycan

gram positive only

63
Q

Vancomycin

What is the primary binding site of Vancomycin?

A

C-terminal D-Ala dipeptide of growing cell wall

multiple residues play a role in interaction with target site

64
Q

Vancomycin

What are the adverse reactions of Vancomycin?

A
  • thrombophlebitis (minimize by using diluted solution and rotate infusion site)
  • flushing due to histamine release
  • ototoxicity and nephrotoxicity (especially when administered with other toxic drugs at these sites)
65
Q

Vancomycin

What can patients being treated with Vancomycin be pre-treated with to prevent flushing?

A

diphenhydramine

other histamine antagonists

66
Q

Vancomycin

What drugs are second generation glycoproteins?

A
  • telavancin
  • dalbavancin
  • oritavancin

semi-synthetic glycopeptides

67
Q

Vancomycin

What is the spectrum of action of Daptomycin?

A

gram (+)

typically for soft tissue infection or endocarditis

68
Q

Vancomycin

Why can Daptomycin not be used for lung infections?

A

deactivated by lung surfactants

69
Q

Vancomycin

What are the adverse effects of Daptomycin?

A

myopathy

little to no ototoxicty or nephrotoxicity

70
Q

Vancomycin

What is the mechanism of action of Daptomycin?

A

daptomycin binds to cytoplasmic membrane then forms complexes in a calcium-dependent manner. complex formation causes rapid loss of cellular potassium resulting in arrest of DNA, RNA, and protein synthesis= cell death

71
Q

Antimycobacterial

What are the difference of mycolic acid in the membrane of mycobacteria versus regular fatty acids?

A
  • decreased membrane permeability
  • stabilizes the membrane
  • less flexibility of the membrane
  • increased survival in harsh conditions
72
Q

Antimycobacterial

What drugs are Rifamycins?

A
  • rifampin
  • rifabutin
  • rifapentine

combo product: isoniazid + rifampin

73
Q

Antimycobacterial

What is the mechanism of action of Rifamycins?

A

inhibits bacterial DNA-dependent RNA polymerase (DDRP) aka RNA polymerase (RNAP) ultimately leading to the termination of RNA elongation

binds “rifampicin binding pocket”

74
Q

Antimycobacterials

What is the use of Rifampin?

A

treatment of mycobacterial infections

75
Q

Antimycobacterial

What are the adverse effects of Rifampin?

A
  • orange discoloration of body fluids like tears, sweat, saliva, urine, and feces
  • constipation
  • hepatotoxicity
76
Q

Antimycobacterial

What antimycobacterial drug induces CYP3A4?

A

Rifamycins

can increase the metabolism of other drugs metabolized by this enzyme

77
Q

Antimycobacterial

Which Rifamycin is the preferred treatment in HIV patients?

A

Rifabutin

milder inducer of CYP3A4

78
Q

Antimycobacterial

What is the use of Fidoxamicin?

A

C. diff infections

low absorption, lower stress on gut microbiome

79
Q

Antimycobacterial

What is the use of Isoniazid?

A

tuberculosis, combo treatment in active cases or preventative treatment in high risk populations (HIV + patients)

WHO list of essential medications

80
Q

Antimycobacterial

What antimycobacterial drug is a CYP450 inhibitor?

A

Isoniazid

81
Q

Antimycobacterial

What is the mechanism of action of Isoniazid?

A

inhibitor of InhA (mycobacterium tuberculosis enoyl reductase)

irreversible

82
Q

Antimycobacterial

What vitamin may become depleted during Isoniazid therapy?

A

vitamin B6

supplementation, severe depletion possible= seizures, acidosis, death

83
Q

Antimycobacterial

What population may be at risk of hepatotoxicity on Isoniazid therapy?

A

slow acetylators

84
Q

Antimycobacterial

What is the half life of Isoniazid?

A

30 mins-5 hours, dependent on NAT2 gene

85
Q

Antimycobacterial

What is the use of Bedaquiline?

A

multi-drug resistant tuberculosis

resistant to isoniazid and rifampicin

86
Q

Antimycobacterial

What is the half life of Bedaquiline?

A

4-5 months

87
Q

Antimycobacterial

What is the mechanism of action of Bedaquiline?

A

binds ATP synthase

88
Q

Antimycobacterial

What is the main route of metabolism of Bedaquiline?

A

CYP3A4

89
Q

Antimycobacterial

What is the mechanism of action of Pyrazinamide?

A

lowers the pH of within the bacterium and macrophages which may interfer with the activity of FAS I, but may directly bind to FAS I to inhibit its activity. also, the acidification of the cell can disrupt the proton motive force which can inhibit ATP production

active compound pyrazinoic acid

90
Q

Antimycobacterial

What is the use of Pyrazinamide?

A

particularly active against dormant or semi-dormant M. tuberculosis in macrophages

91
Q

Antimycobacterial

What is the mechanism of resistance to Pyrazinamide?

A

mutation of pncA gene in mycobacterium

92
Q

Antimycobacterial

What are the side effects of Pyrazinamide?

A

increase in uric acid may cause gout

93
Q

Antimycobacterial

What is the use of Ethambutol?

A

primarly M. tuberculosis, but some activity against mycobacterium avium complex (MAC)

94
Q

Antimycobacterial

How is Ethambutol metabolized?

A

some by the liver, but mostly excreted unchanged so renal dysfunction may lead to increased risk of toxicity

95
Q

Antimycobacterial

What is the adverse effect of Ethambutol?

A

optic neuritis (decreased visual acuity and color blindness)

reversible

96
Q

Antimycobacterial

What is the use of Pretomanid?

A

extensively drug resistant (XDR) or multi-drug resistant M. tuberculosis

typically in combo with bedaquiline and linezolid

97
Q

Antimycobacterial

What is the mechanism of action of Pretomanid?

A

M. Tuberculosis is found in hypoxic enviroments which enhances reduction of pretomanid’s nitro group by nitroreductases= reactive N species cause damage to bacterial proteins, lipids, and DNA

inhibit mycolic acid synthesis via inhib hydroxy-mycolate to ketomycolat

98
Q

Antimycobacterial

What are the second line treatment of tuberculosis?

A
  • levofloxacin
  • carpreomycin
  • moxifloxacin
  • linezolid
  • aminosalicyclic acid
  • cycloserine
  • ethionamide
99
Q

Antimycobacterial

What tuberculosis drug is PABA-like?

A

aminosalicylic acid

folic acid synthesis precursor

100
Q

Antimycobacterial

What is the connection between tuberculosis and vitamin D?

A

patients with TB have lower serum vitamin D levels and may be given in adjunct

no difference in treatment outcomes

101
Q

Antimycobacterial

What are the drugs used for the treatment of Leprosy?

A
  • clofazimine
  • dapsone
  • rifampin
  • thalidomide
102
Q

Antimycobacterial

What is the mechanism of action of Clofazimine?

A
  1. binds to guanine-rich sequence of mycobacterium DNA= stops mycobacterial DNA replication
  2. activates mycobacterial phospholipase A2= increased accumulation of lysophospholipids
103
Q

Antimycobacterial

What is the mechanism of action of Dapsone?

A
104
Q

Antimycobacterial

What is the mechanism of action of Thalidomide?

A

thalidomide -> (arene oxide intermediate) is susceptible to neutophilic attacks and can bind DNA

105
Q

Antimycobacterial

What is the use of Thalidomide?

A

Erthema Nodosum Leprosum(ENL), inflammation of the skin associated with leprosy

106
Q

Antimycobacterial

In what population should Thalidomide be avoided?

A

pregnant patients

107
Q

Oxazolidinone

What is the mechanism of action of Linezolid?

A

Binds specific sites on 23S rRNA within the 50S subunit- prevent complex formation with 70S

108
Q

Oxazolidinone

What is the spectrum of action of Linezolid?

A

-gram positive, including vancomycin resistant Enterococcus faecium (VRE)and MRSA
-nosocomial (hospital) pneumonia and community acquired pneumonia
-skin infections

109
Q

Oxazolidinone

What is the spectrum of action of Tedizolid?

A

-skin infections caused by S aureus (including MRSA and MSSA)
-streptococcus spp.
-Enterococcus spp.

110
Q

Oxazolidinone

Which Oxazolidonone is most likely to cause serotonin syndrome?

A

Linezolid

non-selective MAO inhibitor, Tedizolid less likely

111
Q

Oxazolidinone

Which Oxazolidinone can cause myelosuppression?

A

Linezolid

Tedizolid may also cause it but less likely

112
Q

Oxazolidinone

What is the mechanism of resistance of Oxazolidinone?

A

methylation of adenosine sterically hinders binding to the 23S rRNA

mutation, Linezolid most susceptible to resistance

113
Q

Oxazolidinone

What are the drug interactions of Linezolid/Tedizolid?

A
  • serotonergic agent (risk of serotonin syndrome)
  • foods high in tyramine
114
Q

Plueromutilins

What is the mechanism of action of Retapamulin?

A

binds to bacterial ribosome with high affinity to inhibits ribosomal peptidyl transferase activity and partially inhibit the binding of the initiator tRNA substrate to the ribosome P-site

115
Q

Pleuromutilins

What is the spectrum of action of Retapamulin?

A

-gram positive aerobic bacteria
-impetigo caused by Staph aureus (MSSA) and Streptococcus spp.

116
Q

Pleuromutilins

What is the spectrum of action of Lefamulin?

A
  • gram positive
  • gram negative
  • atypical organism
  • community acquired bacterial pneumonia (CABP)
117
Q

What is the mechanism of action of Mupirocin?

A

reversible inhibitor of bacterial isoleucyl-tRNA synthase= inhibits bacterial protein synthesis

118
Q

What is the spectrum of action of Mupirocin?

A
  • gram positive (including MSSA, MRSA, and Strept. pyogenes)
  • skin infections due to Staph. and Strept.
119
Q

What is the mechanism of action of Clindamycin?

A

prevents peptide bond formation thereby inhibiting protein synthesis by reversibly binding 50S subunit

120
Q

What is the spectrum of action of Clindamycin?

A

aerobic or anaerobic gram positive cocci

more active than erythromycin against anaerobic bacteria

PDA 3 (5 decks)

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