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Pharmacology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Why is it important for GM+ bacteria to have constant cell wall synthesis?

A

They produce autolysins

If there is no synthesis occuring, the autolysins will damage the cell

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2
Q

cell wall inhibitors are only active when the cell is ________ _________.
Name the 2 examples.

A

actively growing

penicillins and cephalosporins

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3
Q

Name 2 penicillinase-resistant penicillins

A

methicillin

cloxacillin

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4
Q

Name 2 extended spectrum penicillins

A

ampicillin

amoxicillin

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5
Q

What is the only penicillin that is IV only?

A

tazo/piperacillin

also, available as IM

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6
Q

Which penicillins are only available as oral doses?

A
  • penicillin v

- amoxicillin

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7
Q

Describe the absorption penicillin?

A
  • partially absorbed –> alter the microflora
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8
Q

Describe the distribution and excretion of penicillin?

A
  • throughout the body
  • crosses placenta
  • stays out of bone and CNS
  • excreted in urine and breast milk
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9
Q

What are the adverse effects of penicillins?

A
  • GI
  • allergy to penicilloic acid (metabolite)
    • rash, lip/tongue swelling, anaphylaxis
  • cross allergy of penicillin class
  • reduced coagulations (caution for anti-coagulant pts)
  • doesn’t affect fetus
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10
Q

Name 5 Cephalosporins

A
  • cephalexin
  • cefuroxime
  • cefazolin
  • cefotaxime
  • ceftriaxone
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11
Q

Cephalosporins are usually administered through IV/IM due to poor oral absorption. Which cephalosporins are given orally?

A
  • cephalexin

- cefuroxime

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12
Q

Describe the distribution of cephalosporins

A
  • cefazolin penetrates bones
  • cefuroxime crosses BBB
  • cefotaxine, ceftriaxone penetrate CSF
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13
Q

Describe the excretion of cephalosporins

A
  • mostly excreted in the urine

- ceftriaxone in bile

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14
Q

What is unique about ceftriaxone?

A
  • it has the longest half-life of all the cephalosporins (6-8 hours)
  • allows the dose to be just once daily
  • excreted in bile (all other cephs excreted through urine)
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15
Q

What are the side effects of cephalosporins?

A
  • cross resistance and cross allergic potential with other cephalosporins and penicillins (similar structure)
  • allergy and GI effects less likely than penicillins
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16
Q

What is the mechanism of vancomycin?

A
  • binds the D-ala, D-ala side chain

- prevents the transglycosylation step of peptidoglycan synthesis

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17
Q

How is vancomycin administered?

A
  • topically

- slow infusion (IV) for systemic infection

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18
Q

How is vancomycin excreted?

A

through urine

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19
Q

What are the side effects of vancomycin?

A
  • fever, chills, phlebitis
  • rapid infusion can cause shock from histamine release
  • hearing loss from drug accumulation (kidney disease pts)
  • toxic when combined with aminoglycosides
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20
Q

What do protein synthesis inhibitor antibiotics attack?
What kind of organisms are they effective against?
Give 5 examples.

A
  • the 70s ribosome in bacteria (as opposed to 80s in mammalian cells)
  • effective against GM+/- and other microorganisms
  • tetracyclines, aminoglycosides, macrolides, chloramphenicol, clindamycin
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21
Q 
What protein synthesis inhibitor is IV only?
What class of drug is this?
A

Gentamicin

aminoglycoside

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22
Q

Describe the mechanism of tetracyclines.

A
  • binds irreversibly to the 30s ribosome
  • inhibits the acyl-tRNA access to ribosome
  • broad spectrum, bacteriostatic
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23
Q

What is the naturally occurring tetracycline?

The 3 semi-synthetics?

A
  • tetracylcine
  • minocycline
  • doxycycline
  • methacycline
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24
Q

What is the administration of tetracyclines?

Absorption?

A
  • orally
  • absorbed adequately, but incompletely
  • absorption reduced by dairy products and antacids
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25
Q

Describe the distribution of tetracyclines?

A
  • concentrates in kidney, liver and spleen
  • crosses placenta
  • penetrates bone and teeth
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26
Q

How are tetracyclines excreted?

A
  • as glucuronides in bile (liver)
  • in urine from glomerular filtration
  • in breast milk
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27
Q

What are the side effects of tetracyclines?

A
  • GI (food prevents this)
  • accumulation in bones/teeth of children
  • hepatotoxicity
  • nausea, vomiting, dizziness
  • sunburn
  • headache/blurred vison
  • superinfection –> due to common resistance
  • NOT FOR kidney/liver pts or pregnant/breastfeeding
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28
Q

What is the mechanism of aminoglycosides?

A
  • protein synthesis inhibitor
  • binds irreversibly to 30s ribosome
  • effective against aerobic GM- bacteria
  • bactericidal
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29
Q

Which aminoglycosides are derived from streptomyces?

micromonospora?

A
  • streptomycin
  • kanamycin
  • amikacin
  • gentamicin
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30
Q

How are aminoglycosides adminstered?

A
  • IV/IM

- sometimes topically

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31
Q

Describe the distribution of aminoglycosides.

A
  • tissue levels are low
  • concentrates in inner ear and renal cortex
  • low amounts in CSF
  • crosses into placenta and enters fetal circulation
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32
Q

How are aminoglycosides excreted?

A

through urine.

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33
Q

What are the side effects of aminoglycosides?

A
  • nephrotoxicity
  • ototoxicity –> destruction of hair cells
  • neuromuscular paralysis
    • toxicity from high dose injections
  • allergy (contact dermatitis from topical neomycin)
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34
Q

Describe the mechanism of macrolides?

A
  • binds irreversibly to 50s ribosome
  • blocks peptidyl transfer
  • broad spectrum, effective against GM+
  • bacteriostatic, bactericidal at high doses
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35
Q

Which macrolides are derived from streptomyces?

Which one is a synthetic ketolide?

A
  • erythromycin
  • azithromycin
  • clarithromycin
  • telithromycin
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36
Q

How are macrolides administered?

Which one is available as an IV infusion?

A
  • orally

- azithromycin can be IV

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37
Q

How are macrolides absorbed?

A
  • adequately absorbed, but food interferes

- erythromycin is destroyed by stomach acid –> must be enteric coated

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38
Q

Describe the distribution of macrolides.

A
  • throughout body
  • does NOT penetrate CSF
  • concentrates in liver
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39
Q

How are macrolides excreted?

A
  • bile

- the inactive metabolites are excreted in the urine

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40
Q

What are the side effects of macrolides?

A
  • GI issues –> most common
  • hepatotoxicity (do not use in liver pts)
  • ototoxicity
  • prolonged QT interval (don’t use in arrhythmia pts)
  • myopathy (interacts with statins)
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41
Q

What is the mechanism for clindomycin?

A
  • protein synthesis inhibitor
  • irreversibly binds to 50s ribosome –> block peptidyl transfer
  • bacteriostatic
  • effective against aerobic/anaerobic GM+ cocci
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42
Q

How is clindamycin administered?

A
  • orally and topically
  • tastes bad –> not for kids
  • topical is for vaginal and acne
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43
Q

Describe the distribution of clindamycin.

A
  • goes throughout body
  • does NOT penetrate CSF or brain
  • concentrates in liver
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44
Q

How is clindamycin excreted?

A
  • in urine and bile
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45
Q

What is the mechanism of penicillins?

A
  • block last step of bacteria cell wall synthesis
  • inhibits transpeptidase from forming cross-links (no structural integrity)
  • causes osmotic pressure –> lysis
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46
Q

What is the mechanism of chloramphenicol?

A
  • protein synthesis inhibitor
  • irreversibly binds to 50s ribosome
  • blocks peptidyl transfer
  • broad spectrum
  • bacteriostatic, bactericidal at high doses
47
Q

How is chloramphenicol administered?

Absorption?

A
  • oral
  • IV
  • topically (eyedrops)
  • absorbed adequately, but food interferes
48
Q

Describe the distribution of chloramphenicol.

A
  • highly lipid soluble

- penetrate CSF and BBB –> can treat brain abcesses

49
Q

How is chloramphenicol excreted?

A
  • in bile as glucuronides

- breast milk

50
Q

What are the side effects of chloramphenicol?

A
  • hemolytic anemia
  • gray baby syndrome
  • drug interactions
    • mycins, warfarin, acetaminophen, rifampin
  • myopathy
    • interacts with statins
51
Q

Describe the mechanism of flouroquinolones.

A
  • DNA synthesis inhbitor
  • Blocks DNA synthesis and induces DNA cleavage
  • bactericidal
  • the “floxacins”
52
Q

Describe the administration and absorption of flouroquinolones.

A
  • oral, IV
  • absorption is good
    • 85-95% absorbed orally
    • calcium may interfere
53
Q

How are flouroquinolones distributed?

Excreted?

A
  • high levels in bone, kidney and prostate
  • low penetration of CSF
  • crosses placenta and enters fetal circulation
  • urine
54
Q

What are the side effects of flouroquinolones?

A
  • GI –> common
  • CNS (headache, dizziness, lightheaded)
  • phototoxicity
  • cartilage erosion (don’t use in pregnant/lactation)
55
Q

What is ciprofloxacin most commonly used for?

A
  • respiratory tract
  • urinary tract
  • bone/joint infections
56
Q

Describe the absorption of cipro?

A
  • 85-95% absorbed (because it’s a flouroquinolone)

- if taken with calcium, Mg, antacids or zinc absorption is reduced (think multivitamins)

57
Q

What does cipro interact with?

A
  • alters levels of drugs metabolized by CYP1A2
  • warfarin –> increased
  • NSAIDS –> seizure risk
  • decreased renal clearance of drugs (ex. methotrexate)
58
Q

What is levofloxacin commonly used for?

A
  • respiratory tract (pneumonia/bronchitis)
  • urinary tract
  • skin infections
59
Q

What does levofloxacin interact with?

A
  • alters level of drugs metabolized by CYP1A2
  • warfarin –> increased levels
  • NSAIDS –> increased seizure risk
  • should not by combined with drugs that prolong the QT wave
  • corticosteriods –> increased risk of tendon rupture
60
Q

What forms are available for moxifloxacin?

What is it commonly used for?

A
  • eye drops, IV, oral
  • respiratory (including TB)
  • endocarditis
  • meningitis
  • conjuctivitis
61
Q

What affects the absorption of moxifloxacin?

A
  • aluminum or magnesium ions
62
Q

What is the main side effect of moxifloxacin?

A
  • may prolong the QT interval

- caution with arrhythmia patients

63
Q

What does moxifloxacin interact with?

A
  • warfarin –> increased levels

- only flouroquinolone that doesn’t interfere with P450 enzymes

64
Q

How do metabolite synthesis inhibitors work?

what are 2 examples?

A
  • work by competitively inhibiting essential metabolites
  • structurally similar to necessary metabolite but doesn’t perform the required metabolic function
  • sulfonamides
  • trimethoprim
65
Q

What mechanisms do sulfonamides have?

A
  • prevent synthesis of dihydrofolic acid
  • broad spectrum (GM+/-)
  • bacteriostatic
66
Q

How can bacteria be resistant to sulfonamides?

A

If they obtain folate from the environment, then sulfonamides won’t work

67
Q

Describe how sulfonamides can be administered.

How are they absorbed?

A
  • oral
  • IV
  • topical
  • absorbed in the small intestine
68
Q

Describe the distribution of sulfonamides.

A

-

69
Q

Describe the distribution of sulfonamides.

A
  • throughout body
  • crosses BBB and penetrates CSF
  • crosses placenta into fetal circulation
70
Q

How are sulfonamides excreted?

A
  • active/inactive metabolites in urine

- breast milk

71
Q

What are the side effects of sulfonamides?

A
  • allergy –> rashes are common
  • kernicterus –> bilirubin in the CNS of newborns
  • nephrotoxicity –> precipitation of drugs, crystals
  • hemolytic anemia
72
Q

What do sulfonamides interact with?

A
  • tolbutimide –> increased hypoglycemic effect

- warfarin –> increased levels

73
Q

What mechanisms does trimethoprim have?

A
  • inhibits the synthesis of tetrahydrofolic acid
  • broad spectrum (GM+/-)
  • bacteriostatic
  • metabolite synthesis inhibitor
74
Q

What is trimethoprim commonly used for?

A
  • urinary tract infections
  • vaginal infections
  • bacterial prostatitis
  • prophylaxis
75
Q

Describe the administration and absorption of trimethoprim

A
  • given orally

- absorbed in small intestine

76
Q

Describe the distribution and excretion of trimethoprim.

A
  • throughout body
  • penetrates CSF
  • crosses placenta and affects fetal folate metabolism
  • urine
77
Q

What are the side effects of trimethoprim?

A
  • miscarriage –> CI

- thrombocytopenia (low platelets) –> risk in pregnancy and poor diets

78
Q

What does trimethoprim interact with?

A

Warfarin –> increased levels

79
Q

What is cotrimoxazole?

What is its mechanism?

A
  • a combo drug made of trimethoprim:sulfonamethoxazole (1:5)
  • synergistic drug that sequentially inhibits folate synthesis
  • bacteriostatic
80
Q

What is cotrimoxazole used for?

A
  • urinary tract
  • respiratory tract
  • GI infections
  • kidney infections
  • prophylaxis in HIV pts
  • septicaemia
81
Q

Describe the administration and absorption of cotrimoxazole.

A
  • given orally or as IV

- absorbed in small intestine

82
Q

Describe the distribution and excretion of cotrimoxazole.

A
  • goes throughout body
  • crosses BBB very slowly
  • crosses placenta and affects fetal folate metabolism
  • excreted in the urine
83
Q

What are the side effects of cotrimoxazole?

A

MANY - not usually given due to the extreme SEs

  • Kernicterus –> CI in pregnancy
  • Hematologic
  • severe rashes
  • nausea/vomiting
  • jaundice, renal damage/failure
  • diarrhea
84
Q

What does cotrimoxazole interact with?

A
  • warfarin –> increased levels

- methotrexate

85
Q

What is the most important component of metronidazole?

Why? What is its mechanism?

A
  • the nitro group –> binds to DNA and inhibits synthesis while also damages the DNA –> cell death
  • bactericidal
  • DOC for amebic infections
86
Q

What is metronidazole used for?

A

anaerobic bacterial infections

87
Q

Describe the administration and absorption of metronidazole.

A
  • oral and topical

- absorbed in small intestine

88
Q

Describe the distribution and excretion on metronidazole.

A
  • throughout the body tissues and fluids
  • crosses BBB and penetrates CSF
  • therapeutic levels in vagina and semen
  • found in breast milk
  • excreted in urine
89
Q

What are the side effects of metronidazole?

A
  • metallic taste in mouth
  • skin irritation/dryness
  • GI effects
  • dizziness/vertigo
  • WHO lists it as a potential carcinogen
90
Q

What does metronidazole interact with?

A

alcohol –> causes tachycardia and shortness of breath

mebendazole –> toxic epidermal necrolysis

91
Q

What are the 4 genetic antibiotic resistance mechanisms?

A
  • inherited resistance
  • acquired resistance
    • vertical evolution
    • horizontal evolution
92
Q

What is inherent resistance?

Give examples.

A
  • natural resistance to an antibiotic
  • doesn’t have target the antibiotic is looking for
  • no transport system into organism
  • resistant to the antibiotic it produces
93
Q

How does vertical evolution contribute to antibiotic resistance?

A
  • non-mutated organisms are killed off
  • resistant organisms thrive and multiply
  • driven by natural selection
94
Q

How does horizontal evolution contribute to antibiotic resistance?

A
  • caused by acquisition of genes from other organisms
  • genetic transfer of resistant DNA between bacteria
  • genetic transfer between virus and bacteria
95
Q

When DNA comes from the environment after being released from another cell (plasmids) this is called _______________.

A

transformation

96
Q

When a virus transfers DNA between bacteria, this is called _______________.

A

transduction

97
Q

Contact between cells as DNA is passed from donor to recipient is called ______________.

A

conjugation

98
Q

What are 6 mechanisms of acquired resistance?

A
  1. conformational change in the antibiotic binding protein
  2. changes in ribosome
  3. resistance genes
  4. antibiotic degrading enzymes
  5. decreased uptake of antibiotic
  6. increased efflux of antibiotic
99
Q

What are the 3 major beta-lactam resistance mechanisms?

A
  1. beta-lactamases (in the periplasmic space)
  2. beta-lactam efflux pumps
  3. beta-lactam resistant cell wall transpeptidases (PBPs)
100
Q

What are the 3 ways to overcome beta-lactam resistance?

A
  1. produce inhibitors of beta-lactamase
    • synergistic effect
  2. combine with other antibiotics
    • bacteria can’t resist both therapies
  3. add bulky side groups to the aromatic ring
    • inhibits enzyme access to the ring
101
Q

What is a predisposing factor that can create VRE colonization?

A
  • using a broad spectrum antibiotic with poor activity
102
Q

What can you do to combat VRE?

A
  • prevention
  • quinupristin/dalfopristin (synercid)
  • linezolid
    • protein synthesis inhibitor
103
Q

Why is linezolid a “reserve antibiotic”?

A
  • only for VREs and MDR bacteria
  • short term drug
  • toxic to mitochondria
104
Q

What mechanism is used for tetracycline resistance?

A
  • Mg2+ gated efflux pump controlled by the TetA gene
105
Q

Describe the mechanisms used in aminoglycoside resistance.

A
  1. Decreased uptake
    • decreased porins
    • lack of oxygen-mediated transport system
  2. Inactivating enzymes
    • acetyl-, nucleotidyl- and phosphotransferases
  3. Cross-resistance is rare
106
Q

Describe the mechanisms used in macrolide resistance.

A
  1. decreased uptake
  2. increased efflux
  3. reduced affinity for 50S ribosome (due to methylation of an adenine)
  4. inactivating enzymes
    • erythromycin esterase
  5. cross-resistance is common
107
Q

Describe the mechanisms used in clindamycin resistance.

A
  • increased efflux
  • reduced affinity for the 50S ribosome (due to methylation of an adenine)
  • cross resistance with macrolides
108
Q

Describe the mechanisms used in chloramphenicol resistance.

A
  • decreased uptake (due to decreased membrane permeability)
  • reduced affinity for 50S ribosome (methylation of adenine)
  • inactivation enzymes
    • chloramphenicol acetyl transferase
109
Q

Describe the mechanisms used in flouroquinolone resistance.

A
  1. alteration of DNA gyrase
  2. reduced uptake
  3. increased efflux
  • cross resistance of quinolones is common
110
Q

Why has flouroquinolone resistance increased so much? (3-fold)

A
  • being prescribed for non-FDA approved uses:
    • ear infections
    • acute respiratory illnesses
    • widespread vet usage
111
Q

Describe the mechanisms used in sulfonamides/trimethoprim resistance?

A
  • if the bacteria obtain folate from the environment
  • mutations of key functional qualities
    • altered dihyrdopteroate synthesis (sulfonamides)
    • altered dihydrofolate synthesis (trimethoprim)
    • decreased permeability to drugs
    • increased production of folate
112
Q

Describe the mechanisms used in cotrimoxazole resistance.

A
  • if bacteria obtain folate from the environment

- resistance is rare since bacteria will have to be resistant to both component of the antibiotic

113
Q

Describe the mechanisms used in metronidazole resistance.

A
  • resistance is rare
  • reoxidation of metronidazole by resistant cells
    • reoxidation = no free radicals of nitro group (main action)
  • reduced uptake

Pharmacology (5 decks)

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