Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Antibiotics > Flashcards

Antibiotics Flashcards

(113 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

actively growing

penicillins and cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name 2 penicillinase-resistant penicillins

A

methicillin

cloxacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name 2 extended spectrum penicillins

A

ampicillin

amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the only penicillin that is IV only?

A

tazo/piperacillin

also, available as IM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which penicillins are only available as oral doses?

A
  • penicillin v

- amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the absorption penicillin?

A
  • partially absorbed –> alter the microflora
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name 5 Cephalosporins

A
  • cephalexin
  • cefuroxime
  • cefazolin
  • cefotaxime
  • ceftriaxone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A
  • cephalexin

- cefuroxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the distribution of cephalosporins

A
  • cefazolin penetrates bones
  • cefuroxime crosses BBB
  • cefotaxine, ceftriaxone penetrate CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the excretion of cephalosporins

A
  • mostly excreted in the urine

- ceftriaxone in bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of vancomycin?

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

- prevents the transglycosylation step of peptidoglycan synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is vancomycin administered?

A
  • topically

- slow infusion (IV) for systemic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is vancomycin excreted?

A

through urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q 
What protein synthesis inhibitor is IV only?
What class of drug is this?
A

Gentamicin

aminoglycoside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the mechanism of tetracyclines.

A
  • binds irreversibly to the 30s ribosome
  • inhibits the acyl-tRNA access to ribosome
  • broad spectrum, bacteriostatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the naturally occurring tetracycline?

The 3 semi-synthetics?

A
  • tetracylcine
  • minocycline
  • doxycycline
  • methacycline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the administration of tetracyclines?

Absorption?

A
  • orally
  • absorbed adequately, but incompletely
  • absorption reduced by dairy products and antacids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe the distribution of tetracyclines?
- concentrates in kidney, liver and spleen - crosses placenta - penetrates bone and teeth
26
How are tetracyclines excreted?
- as glucuronides in bile (liver) - in urine from glomerular filtration - in breast milk
27
What are the side effects of tetracyclines?
- 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
28
What is the mechanism of aminoglycosides?
- protein synthesis inhibitor - binds irreversibly to 30s ribosome - effective against aerobic GM- bacteria - bactericidal
29
Which aminoglycosides are derived from streptomyces? | micromonospora?
- streptomycin - kanamycin - amikacin - gentamicin
30
How are aminoglycosides adminstered?
- IV/IM | - sometimes topically
31
Describe the distribution of aminoglycosides.
- tissue levels are low - concentrates in inner ear and renal cortex - low amounts in CSF - crosses into placenta and enters fetal circulation
32
How are aminoglycosides excreted?
through urine.
33
What are the side effects of aminoglycosides?
- nephrotoxicity - ototoxicity --> destruction of hair cells - neuromuscular paralysis - toxicity from high dose injections - allergy (contact dermatitis from topical neomycin)
34
Describe the mechanism of macrolides?
- binds irreversibly to 50s ribosome - blocks peptidyl transfer - broad spectrum, effective against GM+ - bacteriostatic, bactericidal at high doses
35
Which macrolides are derived from streptomyces? | Which one is a synthetic ketolide?
- erythromycin - azithromycin - clarithromycin - telithromycin
36
How are macrolides administered? | Which one is available as an IV infusion?
- orally | - azithromycin can be IV
37
How are macrolides absorbed?
- adequately absorbed, but food interferes | - erythromycin is destroyed by stomach acid --> must be enteric coated
38
Describe the distribution of macrolides.
- throughout body - does NOT penetrate CSF - concentrates in liver
39
How are macrolides excreted?
- bile | - the inactive metabolites are excreted in the urine
40
What are the side effects of macrolides?
- 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)
41
What is the mechanism for clindomycin?
- protein synthesis inhibitor - irreversibly binds to 50s ribosome --> block peptidyl transfer - bacteriostatic - effective against aerobic/anaerobic GM+ cocci
42
How is clindamycin administered?
- orally and topically - tastes bad --> not for kids - topical is for vaginal and acne
43
Describe the distribution of clindamycin.
- goes throughout body - does NOT penetrate CSF or brain - concentrates in liver
44
How is clindamycin excreted?
- in urine and bile
45
What is the mechanism of penicillins?
- block last step of bacteria cell wall synthesis - inhibits transpeptidase from forming cross-links (no structural integrity) - causes osmotic pressure --> lysis
46
What is the mechanism of chloramphenicol?
- protein synthesis inhibitor - irreversibly binds to 50s ribosome - blocks peptidyl transfer - broad spectrum - bacteriostatic, bactericidal at high doses
47
How is chloramphenicol administered? | Absorption?
- oral - IV - topically (eyedrops) - absorbed adequately, but food interferes
48
Describe the distribution of chloramphenicol.
- highly lipid soluble | - penetrate CSF and BBB --> can treat brain abcesses
49
How is chloramphenicol excreted?
- in bile as glucuronides | - breast milk
50
What are the side effects of chloramphenicol?
- hemolytic anemia - gray baby syndrome - drug interactions - mycins, warfarin, acetaminophen, rifampin - myopathy - interacts with statins
51
Describe the mechanism of flouroquinolones.
- DNA synthesis inhbitor - Blocks DNA synthesis and induces DNA cleavage - bactericidal - the "floxacins"
52
Describe the administration and absorption of flouroquinolones.
- oral, IV - absorption is good - 85-95% absorbed orally - calcium may interfere
53
How are flouroquinolones distributed? | Excreted?
- high levels in bone, kidney and prostate - low penetration of CSF - crosses placenta and enters fetal circulation - urine
54
What are the side effects of flouroquinolones?
- GI --> common - CNS (headache, dizziness, lightheaded) - phototoxicity - cartilage erosion (don't use in pregnant/lactation)
55
What is ciprofloxacin most commonly used for?
- respiratory tract - urinary tract - bone/joint infections
56
Describe the absorption of cipro?
- 85-95% absorbed (because it's a flouroquinolone) | - if taken with calcium, Mg, antacids or zinc absorption is reduced (think multivitamins)
57
What does cipro interact with?
- alters levels of drugs metabolized by CYP1A2 - warfarin --> increased - NSAIDS --> seizure risk - decreased renal clearance of drugs (ex. methotrexate)
58
What is levofloxacin commonly used for?
- respiratory tract (pneumonia/bronchitis) - urinary tract - skin infections
59
What does levofloxacin interact with?
- 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
What forms are available for moxifloxacin? | What is it commonly used for?
- eye drops, IV, oral - respiratory (including TB) - endocarditis - meningitis - conjuctivitis
61
What affects the absorption of moxifloxacin?
- aluminum or magnesium ions
62
What is the main side effect of moxifloxacin?
- may prolong the QT interval | - caution with arrhythmia patients
63
What does moxifloxacin interact with?
- warfarin --> increased levels | - only flouroquinolone that doesn't interfere with P450 enzymes
64
How do metabolite synthesis inhibitors work? | what are 2 examples?
- work by competitively inhibiting essential metabolites - structurally similar to necessary metabolite but doesn't perform the required metabolic function - sulfonamides - trimethoprim
65
What mechanisms do sulfonamides have?
- prevent synthesis of dihydrofolic acid - broad spectrum (GM+/-) - bacteriostatic
66
How can bacteria be resistant to sulfonamides?
If they obtain folate from the environment, then sulfonamides won't work
67
Describe how sulfonamides can be administered. | How are they absorbed?
- oral - IV - topical - absorbed in the small intestine
68
Describe the distribution of sulfonamides.
-
69
Describe the distribution of sulfonamides.
- throughout body - crosses BBB and penetrates CSF - crosses placenta into fetal circulation
70
How are sulfonamides excreted?
- active/inactive metabolites in urine | - breast milk
71
What are the side effects of sulfonamides?
- allergy --> rashes are common - kernicterus --> bilirubin in the CNS of newborns - nephrotoxicity --> precipitation of drugs, crystals - hemolytic anemia
72
What do sulfonamides interact with?
- tolbutimide --> increased hypoglycemic effect | - warfarin --> increased levels
73
What mechanisms does trimethoprim have?
- inhibits the synthesis of tetrahydrofolic acid - broad spectrum (GM+/-) - bacteriostatic - metabolite synthesis inhibitor
74
What is trimethoprim commonly used for?
- urinary tract infections - vaginal infections - bacterial prostatitis - prophylaxis
75
Describe the administration and absorption of trimethoprim
- given orally | - absorbed in small intestine
76
Describe the distribution and excretion of trimethoprim.
- throughout body - penetrates CSF - crosses placenta and affects fetal folate metabolism - urine
77
What are the side effects of trimethoprim?
- miscarriage --> CI | - thrombocytopenia (low platelets) --> risk in pregnancy and poor diets
78
What does trimethoprim interact with?
Warfarin --> increased levels
79
What is cotrimoxazole? | What is its mechanism?
- a combo drug made of trimethoprim:sulfonamethoxazole (1:5) - synergistic drug that sequentially inhibits folate synthesis - bacteriostatic
80
What is cotrimoxazole used for?
- urinary tract - respiratory tract - GI infections - kidney infections - prophylaxis in HIV pts - septicaemia
81
Describe the administration and absorption of cotrimoxazole.
- given orally or as IV | - absorbed in small intestine
82
Describe the distribution and excretion of cotrimoxazole.
- goes throughout body - crosses BBB very slowly - crosses placenta and affects fetal folate metabolism - excreted in the urine
83
What are the side effects of cotrimoxazole?
MANY - not usually given due to the extreme SEs - Kernicterus --> CI in pregnancy - Hematologic - severe rashes - nausea/vomiting - jaundice, renal damage/failure - diarrhea
84
What does cotrimoxazole interact with?
- warfarin --> increased levels | - methotrexate
85
What is the most important component of metronidazole? | Why? What is its mechanism?
- the nitro group --> binds to DNA and inhibits synthesis while also damages the DNA --> cell death - bactericidal - DOC for amebic infections
86
What is metronidazole used for?
anaerobic bacterial infections
87
Describe the administration and absorption of metronidazole.
- oral and topical | - absorbed in small intestine
88
Describe the distribution and excretion on metronidazole.
- 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
What are the side effects of metronidazole?
- metallic taste in mouth - skin irritation/dryness - GI effects - dizziness/vertigo - WHO lists it as a potential carcinogen
90
What does metronidazole interact with?
alcohol --> causes tachycardia and shortness of breath | mebendazole --> toxic epidermal necrolysis
91
What are the 4 genetic antibiotic resistance mechanisms?
- inherited resistance - acquired resistance - vertical evolution - horizontal evolution
92
What is inherent resistance? | Give examples.
- 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
How does vertical evolution contribute to antibiotic resistance?
- non-mutated organisms are killed off - resistant organisms thrive and multiply - driven by natural selection
94
How does horizontal evolution contribute to antibiotic resistance?
- caused by acquisition of genes from other organisms - genetic transfer of resistant DNA between bacteria - genetic transfer between virus and bacteria
95
When DNA comes from the environment after being released from another cell (plasmids) this is called _______________.
transformation
96
When a virus transfers DNA between bacteria, this is called _______________.
transduction
97
Contact between cells as DNA is passed from donor to recipient is called ______________.
conjugation
98
What are 6 mechanisms of acquired resistance?
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
What are the 3 major beta-lactam resistance mechanisms?
1. beta-lactamases (in the periplasmic space) 2. beta-lactam efflux pumps 3. beta-lactam resistant cell wall transpeptidases (PBPs)
100
What are the 3 ways to overcome beta-lactam resistance?
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
What is a predisposing factor that can create VRE colonization?
- using a broad spectrum antibiotic with poor activity
102
What can you do to combat VRE?
- prevention - quinupristin/dalfopristin (synercid) - linezolid - protein synthesis inhibitor
103
Why is linezolid a "reserve antibiotic"?
- only for VREs and MDR bacteria - short term drug - toxic to mitochondria
104
What mechanism is used for tetracycline resistance?
- Mg2+ gated efflux pump controlled by the TetA gene
105
Describe the mechanisms used in aminoglycoside resistance.
1. Decreased uptake - decreased porins - lack of oxygen-mediated transport system 2. Inactivating enzymes - acetyl-, nucleotidyl- and phosphotransferases 3. Cross-resistance is rare
106
Describe the mechanisms used in macrolide resistance.
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
Describe the mechanisms used in clindamycin resistance.
- increased efflux - reduced affinity for the 50S ribosome (due to methylation of an adenine) - cross resistance with macrolides
108
Describe the mechanisms used in chloramphenicol resistance.
- decreased uptake (due to decreased membrane permeability) - reduced affinity for 50S ribosome (methylation of adenine) - inactivation enzymes - chloramphenicol acetyl transferase
109
Describe the mechanisms used in flouroquinolone resistance.
1. alteration of DNA gyrase 2. reduced uptake 3. increased efflux - cross resistance of quinolones is common
110
Why has flouroquinolone resistance increased so much? (3-fold)
- being prescribed for non-FDA approved uses: - ear infections - acute respiratory illnesses - widespread vet usage
111
Describe the mechanisms used in sulfonamides/trimethoprim resistance?
- 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
Describe the mechanisms used in cotrimoxazole resistance.
- if bacteria obtain folate from the environment | - resistance is rare since bacteria will have to be resistant to both component of the antibiotic
113
Describe the mechanisms used in metronidazole resistance.
- resistance is rare - reoxidation of metronidazole by resistant cells - reoxidation = no free radicals of nitro group (main action) - reduced uptake

Pharmacology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions