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Pharmacology > Antibiotics 2 > Flashcards

Antibiotics 2 Flashcards

1
Q

What 2 classes of Abs are cell wall inhibitors?

A

penicillins and cephalosporins

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2
Q

What are the 2 classes of protein synthesis inhibitors?

A

tetracyclines and macrolides

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3
Q

What is the 1 class of DNA synthesis inhibitors?

A

fluoroquinolones

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4
Q

Targeting the synthesis of _____ is one of the most widely effective and least toxic antibiotic strategies

A

bacterial cell walls

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5
Q

What are cell wall inhibitors only effective against?

A

actively growing bacteria

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6
Q

How does penicillin inhibit cell wall synthesis?

A

it inhibits transpeptidase that forms cross links between peptidoglycan chains that are essential for cell wall integrity
- causes osmotic pressure on the cells resulting in cell lysis

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7
Q

What enzyme does gram positive bacteria product to break down the cell wall?

A
  • produces autolysins
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8
Q

Without active cell wall synthesis ____ can damage the cell

A

autolysins

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9
Q

What are the 2 examples of penicillinase resistant penicillins

A
  • methicillin and cloxacillin
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10
Q

What are the 2 examples of extended spectrum penicillins

A
  • ampicillin and amoxicillin
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11
Q

Are penicillins bactericidal or bacteriostatic?

A

Bacteriocidal

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12
Q

Penicillin V and Amoxicillin are only available as ______

A

oral preparations

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13
Q

Pipercillin must be through the _____ route

A

IV/IM

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14
Q

Why do penicillins affect the composition of the intestinal flora?

A
  • because they are incompletely absorbed
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15
Q

Absorption of penicillinase resistant antibiotics are ___ by food in the stomach and must be administered ______

A

reduced

- before a meal or 2-3 hours after

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16
Q

Does penicillin cross the placenta? What abut the bone or CNS?

A
  • does cross the placenta

- does not penetrate the bone or CNS

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17
Q

Where is penicillin excreted?

A
  • in the urine and breast milk
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18
Q

What are the most common adverse effects of penicillins?

A
  • GI effects relatively common but are seldom severe due to the disruption of normal intestinal microflora
  • allergy to its metabolite penicilloic acid relatively common (rash, swelling, anaphylaxis)
  • cross allergy within the penicillin class
  • no negative birth effects
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19
Q

_____ is a concern in patients receiving anticoagulants also also on penicillin

A

Reduced coagulation

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20
Q

What are the 4 antibiotics that fall under the class of cephalosporins?

A

cephalxin, cephalothin, cepazolin, cefepime

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21
Q

Which cephalosporins are the only 2 Abs administered orally?

A
  • cephalexin and cefixime
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22
Q

____ penetrates the bone

A

cefazolin

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23
Q

____ crosses the BBB

A

cefuroxime

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24
Q

____ and _____ penetrate the cerebrospinal fluid

A

cefotaxime and ceftriaxone

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25
Q

Where are most cephalosporins excreted?

A
  • most are eliminated in the urine

cefriaxone is excreted in the bile- longest t1/2 of all cephalosporins

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26
Q

How do protein synthesis inhibitors work?

A

Bind to 70S ribosomes (in bacterial cells) opposed to the 80S ribosomes that are in mammalian cells
- effective against gram positive and gram negative bacteria as well as other micro organisms

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27
Q

What are the 5 classes of antibiotics that fall under the protein synthesis inhibitors class?

A
  • tetracyclines
  • amino-glycosides
  • macrolides
  • chloramphenicol
  • clindamycin
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28
Q

How do tetracyclines act as a protein synthesis inhibitor?

A
  • binds irreversible to the 30S ribosome

- blocks acyl-tRNA access to the ribosome

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29
Q

Tetracyclines are considered ____ spectrum and are bacterio____

A

broad

bacteriostatic

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30
Q

What is the naturally occurring tetracycline?

A

tetracycline

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31
Q

What is the semi-synthetic tetracyclines?

A
  • doxycycline
  • methacycline
  • minocycline
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32
Q

Absorption PO of tetracycline is reduced by the consumption of ____ and ____

A

dairy foods and antacids

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33
Q

Describe the distribution of tetracyclines. Where do they concentrate? What do they cross?

A
  • distribution is throughout the body and body fluids
  • concentrates in the liver, kidney, and spleen
  • crosses the placenta and penetrates the bone and teeth
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34
Q

Where are tetracyclines excreted?

A
  • metabolized and conjugated to form glucuronides by the liver and secreted in the bile and enters the urine via glomerular filtration
  • excreted as well in the breast milk
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35
Q

What are the adverse effects of tetracyclines?

A
  • GI discomfort- overcome by consuming food with the pills
  • deposition in bones and teeth of growing children
  • hepatotoxicity
  • sunburn (increased sensitivity to UV rays)
  • dizziness, nausea and vomiting
    (minocycline and doxycycline concentrate in the inner ear)
  • headache/blurred vision
  • superinfection: resistance is common
  • not recommended or patients with kidney/liver disease or pregnant/lactating women
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36
Q

How do aminoglycosides act as a protein synthesis inhibitor?

A
  • binds irreversibly to the 30S ribosome

- blocks functional assembly of the ribosome

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37
Q

Amino glycosides are effective against _______

A

aerobic gram negative bacteria

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38
Q

Is aminoglycosides bacteriocidal or bacteriostatic

A

bacteriocidal

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39
Q

What Abs are derived from streptomyces?

A

streptomycin

kanamycin

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40
Q

What Abs are derived from micromonospora?

A

gentamicin

amikacin

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41
Q

Molecular properties of aminoglycosides prevent ____ absorption

A

oral

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42
Q

Describe the distribution of aminoglycosides in the body?

A
  • levels achieved in most tissues are low
  • concentrates in the renal cortex and the inner ear
  • low penetration into the cerebrospinal fluid
  • crosses the placenta and enters the fetal circulation
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43
Q

Where are aminoglycosides excreted?

A

the urine

44
Q

What are the adverse effects associated with aminoglycosides?

A
  • nephrotoxicity - retention of aminoglycosides by proximal tubular cells disrupts calcium mediated transport
  • ototoxicity - deafness caused by the destruction of hair cells within the inner ear (fetuses and elderly are the most susceptible)
  • neuromuscular paralysis- high dose toxicity from injections
  • allergic reactions
45
Q

How do macrolides act as protein synthesis inhibitors?

A
  • bind irreversibly to the 50S ribosome

- blocks peptidyl transfer

46
Q

Macrolides are ____ spectrum and effective against gram ___ bacteria

A

broad

positive

47
Q

What macrolide Abs are derived from streptomyces

A
  • erythromycin
  • clarithromycin
  • azithromycin
48
Q

What macrolides are derived from the synthetic ketolides?

A

telithromycin

49
Q

Macrolides are ____ administered

A

orally

50
Q

___ interferes with the absorption of macrolides.

A

food

51
Q

What is one method of ensuring that erythromycin does not get destroyed in the gastric acid of the stomach?

A

can enteric coat the tablets

52
Q

Describe the distribution of macrolide Abs?

A
  • distributes throughout the body
  • does not penetrate the cerebrospinal fluid
  • concentrates in the liver
53
Q

Where are macrolide Abs excreted? What about their inactive metabolites?

A
  • excreted in the bile

- inactive metabolites are secreted in the urine

54
Q

What are the adverse effects associated with using macrolides?

A
  • GI problems
  • jaundice
  • ototoxicity (associated with high doses of erythromycin)
  • prolonged QT c interval- patients with existing arrhythmia (erythromycin, clarithromycin)
  • myopathy - interactions with statins due to the inhibition of CYP 3A4
55
Q

In what case would we use Quinupristin/Dalfopristin (synercid)?

A
  • reserved for the treatment of vancomycin resistant enterococcus
  • mixture of 2 drugs in a ratio of 70:30
  • binds to separate sites on the ribosome (Quinupristin binds to the 50S subunit preventing peptide elongation while dalfopristin binds to the 23S subunit preventing peptide transfer
  • tx of gram + cocci
  • bactericidal with a long post Ab effect
56
Q

What is the administration route of synercid

A

IV/IM

57
Q

What is the distribution of synercid?

A
  • penetrates macrophages and polymorphonucleosites- VREs grow intracellularly
  • low levels in the cerebrospinal fluid
58
Q

Where is synercid excreted?

A

in the bile

- secondarily excreted in the urine

59
Q

What are the adverse effects of synercid?

A
  • venous irritation when given IV
  • joint/muscle ache in patients given high doses
  • hyperbilirubinemia (bilirubin is elevated in about 25% of patients)
  • causes inhibition of P450
60
Q

What are the two enzymes that are inhibited by DNA synthesis inhibitors?

A
  • bacterial topoisomerase

- DNA gyrase

61
Q

What are two examples of DNA synthesis inhibitors?

A
  • fluorowuinolones

- rifamycin

62
Q

What enzyme does fluoroquinolones inhibit?

A
  • DNA gyrase
63
Q

What route of administration are fluoroquinolones given?

A
  • via the oral/IV route
64
Q

What mineral interferes with oral absorption of fluoroquinolones?

A
  • dietary calcium
65
Q

What is the distribution of the fluoroquinolones?

A
  • distributes well throughout the tissues
  • levels are high in the bones, kidney and prostate
  • low penetration into the cerebral spinal fluid
  • crosses the placenta and enters fetal circulation
66
Q

Where are fluoroquinolones excreted?

A

the urine

67
Q

List the adverse effects of fluoroquinolones?

A
  • GI disturbances
  • CNS - light headed, dizziness
  • phototoxicity
  • cartilage erosion (should not be administered to pregnant or nursing women)
68
Q

What is the most commonly prescribed fluoroquinolone?

A
  • ciprofloxacin
69
Q

What infections is ciproflxacin generally used to treat?

A
  • infections of the bones/joints
  • infections of the respiratory tract
  • infections of the urinary tract
70
Q

Administration of fluoroquinolones at the same time as ____substantially reduces absorption

A

calcium, antacids, zinc, magnesium

71
Q

What are the drug interactions that ciproflaxacin has?

A
  • alters level of drugs metabolized by the cytochrome P450 enzyme
  • warfarin levels can be dangerously increased
  • increased seizure risk when combines with NSAIDS
  • affects the renal clearance of other drugs such as methotrexate
72
Q

What infections is moxiflaxacin used to treat?

A
  • respiratory tract infections
  • endocarditis
  • meningitis
  • conjunctivitis
73
Q

Concurrent administration of moxifloxacin along with ____ significantly reduced absorption

A
  • aluminum or mangesium
74
Q

What is moxifloxacin’s adverse drug reactions?

A
  • ## may prolong the QTc interval - should not be used in patients with cardiac arrhythmias
75
Q

What drug interactions are associated with moxifloxacin?

A
  • does not inhibit the cut p450 enzyme

- may interact with warfarin

76
Q

What antibacterials ball under the category of metabolite synthesis inhibitors?

A
  • sulfonamides

- trimethoprim

77
Q

Sulfonamides inhibit the synthesis of bacterial _____ acid

A

dihydrofolic acid

78
Q

What bacteria are sulfonamides active against?

A
  • most gram positive and many gram negative bacteria - broad spectrum
79
Q

Bacteria that _________ are inherently resistant for sulfonamides

A

obtain folate from the environment

80
Q

What is considered a short acting sulphonamide?

A
  • sulfamethazole

- sulfadiazine

81
Q

What is considered an intermediate acting sulfonamide?

A
  • sulfacetamide

- sulfadoxine

82
Q

What is considered to be a long acting sulfonamide?

A

sulfadimethoxine

83
Q

Where are sulfonamides absorbed?

A
  • in the small intestine
84
Q

Describe sulfonamide distribution

A
  • crosses the BBB and penetrates the CSF

- crosses the placenta and gets into fetal circulation

85
Q

Where are sulfonamides excreted?

A
  • active and inactive metabolites secreted in the urine

- secreted into the breast milk

86
Q

What are the adverse effects of sulfonamides?

A
  • allergies common
  • kernicterus- sulfonamide displaces bilirubin from binding albumin causing free bilirubin to cross the undeveloped BBB and pass into the CNS
  • nephrotoxicity (solubility of sulfonamides is low)
  • hemolytic anemia
87
Q

What are the drug interactions associated with sulfonamides?

A
  • potentiate the hypoglycaemia effect of tolbutamide

- potentiate the anticoagulant effect of warfarin

88
Q

Trimethoprim inhibits the synthesis of bacterial ______

A

tetrahydrofolic acid

89
Q

What is trimethoprim active against?

A
  • against most gram positive and many gram negative bacteria

- broad spectrum

90
Q

Trimethoprim is used in the treatment of what?

A
  • urinary tract infections
  • vaginal infections
  • bacterial prostatitis
  • prophylaxis
91
Q

Absorption of trimethoprim is where?

A

in the small intestine

92
Q

Where is trimethoprim distributed?

A
  • penetrates CSF
  • crosses the placenta and affects fetal folate metabolism
  • distributed widely throughout the body
93
Q

Where is trimethoprim excreted?

A
  • in the urine
94
Q

What are the adverse effects of trimethoprim?

A
  • contraindicated in pregnancy (doubling of miscarriage rates)
  • thrombocytopenia (low levels of platelets, pregnant women and those with poor diets are at a higher risk
95
Q

What does trimethoprim interact with?

A
  • potentiates the anticoagulant effects of warfarin
96
Q

What 2 medications make up cotrimoxazole?

A
  • composed of both trimethoprim (more lipid soluble) and sulfonamethazole in a 1:5 ratio
97
Q

There is _____ activity in cotrimoxazole from the sequential inhibition of ______

A

synergistic

folate synthesis

98
Q

What is the advantage of using cotrimoxazole over other sulfonamides?

A
  • broader spectrum
99
Q

Cotrimoxazole is used generally in the treatment of what infections?

A
  • urinary tract infections
  • respiratory tract infections
  • kidney infections
  • GI tract infections
  • septicemia
  • prophylaxis in HIV patients
100
Q

Where is cotrimoxazole absorbed?

A

in the small intestine

101
Q

Cotrimoxazole is distributed where in the body?

A
  • throughout the body
  • crosses the BBB very slowly
  • crosses the placenta and affects fetal folate metabolism
102
Q

Where is cotrimoxazole excreted?

A

in the urine

103
Q

What are the adverse effects associated with cotrimoxazole use?

A
  • contraindicated for pregnant women
  • hematologic (thrombocytopenia, anemia, leukopenia)
  • skin rashes are common and can be severe in the elderly
  • nausea/vomiting
  • jaundice, renal damage/ failure
  • rashes/diarrhea (common along immunocompromised patients)
104
Q

What are the drug interactions that are associated with cotrimoxazole?

A
  • potentiate the anti-coagulant effect of warfarin

- methotrexate is displaced for albumin binding sites

105
Q

Normal GI and vaginal flora are disrupted with antibiotic use, contributing to 4 major side effects

A

nausea, vomiting, diarrhea and yeast infections

Pharmacology (23 decks)

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