Micro Flashcards

(32 cards)

1
Q

What are the 5 main mechanisms of antibiotic action? 🦠

A

1️⃣ Inhibition of Cell Wall Synthesis 🧱 (e.g. beta-lactams, glycopeptides)
2️⃣ Inhibition of Protein Synthesis πŸ›‘ (e.g. aminoglycosides, tetracyclines)
3️⃣ Inhibition of Nucleic Acid Synthesis 🧬 (e.g. fluoroquinolones, rifamycins)
4️⃣ Inhibition of Metabolic Pathways 🦠 (e.g. sulfonamides, trimethoprim)
5️⃣ Disruption of Cell Membrane Integrity ⛓️‍πŸ’₯ (e.g. polymyxins, daptomycin)

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2
Q

Give examples of antibiotics that inhibit cell wall synthesis 🧱

A

πŸ”Ή Beta-lactams: penicillin, ceftriaxone, meropenem (bind PBPs)
πŸ”Ή Glycopeptides: vancomycin, teicoplanin (bind D-Ala-D-Ala)
πŸ”Ή Monobactams: aztreonam (Gram-negative only)

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3
Q

Which antibiotics act on the 30S ribosomal subunit? πŸ›‘

A

πŸ”Ή Aminoglycosides (gentamicin, amikacin) – bactericidal
πŸ”Ή Tetracyclines (doxycycline, tigecycline) – usually bacteriostatic

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4
Q

Which antibiotics act on the 50S ribosomal subunit? πŸ›‘

A

πŸ”Ή Macrolides (azithromycin, clarithromycin)
πŸ”Ή Lincosamides (clindamycin)
πŸ”Ή Oxazolidinones (linezolid)

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5
Q

Give examples of antibiotics that inhibit nucleic acid synthesis 🧬

A

πŸ”Ή Fluoroquinolones (ciprofloxacin, levofloxacin) – inhibit DNA gyrase/topoisomerase IV
πŸ”Ή Rifamycins (rifampicin) – inhibit RNA polymerase
πŸ”Ή Nitroimidazoles (metronidazole) – DNA strand breakage

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6
Q

Give examples of antibiotics that inhibit metabolic pathways 🦠

A

πŸ”Ή Sulfonamides – inhibit dihydropteroate synthase
πŸ”Ή Trimethoprim – inhibits dihydrofolate reductase
πŸ’‘ Often combined as co-trimoxazole for synergy

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7
Q

Give examples of antibiotics that disrupt cell membrane integrity ⛓️‍πŸ’₯

A

πŸ”Ή Polymyxins (colistin, polymyxin B) – Gram-negative MDR, nephro/neurotoxic
πŸ”Ή Daptomycin – Gram-positive resistant, inactivated by lung surfactant

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8
Q

What is MIC and why is it important?

A

πŸ’‘ Minimum Inhibitory Concentration: lowest antibiotic concentration that prevents visible bacterial growth.
πŸ“Œ Determines dosing strategies to keep drug above MIC for effective bacterial kill.

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9
Q

What are time-dependent antibiotics? ⏳

A

🧱 Aim: Keep concentration above MIC for as long as possible in dosing interval
πŸ’Š Examples: beta-lactams, vancomycin
πŸ’‘ ICU: prolonged/continuous infusions improve efficacy

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10
Q

What are concentration-dependent antibiotics? πŸ“ˆ

A

πŸ“Œ Aim: High peak:Cmax ratio for best kill
πŸ’Š Examples: aminoglycosides
βœ… Dose once daily to maximise peak and reduce toxicity

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11
Q

What are AUC-dependent antibiotics? πŸ“Š

A

πŸ“Œ Aim: Optimise total exposure (AUC:MIC)
πŸ’Š Examples: fluoroquinolones, vancomycin, linezolid
πŸ’‘ TDM needed for vancomycin (AUC:MIC >400)

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12
Q

What are the 4 major mechanisms of antimicrobial resistance? 🧬

A

1️⃣ Enzymatic degradation/modification (e.g. beta-lactamases)
2️⃣ Altered target site (e.g. MRSA altered PBP2a)
3️⃣ Efflux pumps (e.g. Pseudomonas)
4️⃣ Reduced permeability (e.g. porin loss in Gram-negatives)

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13
Q

Give examples of common resistant organisms in ICU πŸ₯

A

πŸ”Ή MRSA – mecA gene β†’ altered PBP2a
πŸ”Ή VRE – altered peptidoglycan terminus
πŸ”Ή ESBL Enterobacteriaceae – hydrolyse beta-lactams
πŸ”Ή CRE – carbapenemases
πŸ”Ή MDR Pseudomonas & Acinetobacter
πŸ”Ή Azole-resistant Candida (C. auris)

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14
Q

What are the main challenges of fungal infection in ICU? πŸ„

A

🚧 Non-specific presentation
⏳ Delayed/difficult diagnosis
πŸ“ˆ Rising incidence in immunosuppression, devices, TPN
πŸ’Š Limited antifungal options + resistance
⚠️ High mortality

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15
Q
A
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16
Q

What are the 5 main mechanisms of antibiotic action? 🦠

A

1️⃣ Inhibition of Cell Wall Synthesis 🧱 (beta-lactams, glycopeptides, monobactams)
2️⃣ Inhibition of Protein Synthesis πŸ›‘ (aminoglycosides, tetracyclines, macrolides, clindamycin, linezolid)
3️⃣ Inhibition of Nucleic Acid Synthesis 🧬 (fluoroquinolones, rifampicin, metronidazole)
4️⃣ Inhibition of Metabolic Pathways 🦠 (sulfonamides, trimethoprim)
5️⃣ Disruption of Cell Membrane Integrity ⛓️‍πŸ’₯ (polymyxins, daptomycin)

17
Q

Give examples of cell wall synthesis inhibitors 🧱

A

πŸ”Ή Beta-lactams: penicillin, ceftriaxone, meropenem (bind PBPs)
πŸ”Ή Glycopeptides: vancomycin, teicoplanin (bind D-Ala-D-Ala)
πŸ”Ή Monobactams: aztreonam (Gram-negative only)

18
Q

Which antibiotics act on 30S ribosomal subunit? πŸ›‘

A

πŸ”Ή Aminoglycosides (gentamicin, amikacin) – bactericidal
πŸ”Ή Tetracyclines (doxycycline, tigecycline) – bacteriostatic

19
Q

Which antibiotics act on 50S ribosomal subunit? πŸ›‘

A

πŸ”Ή Macrolides (azithromycin, clarithromycin)
πŸ”Ή Lincosamides (clindamycin)
πŸ”Ή Oxazolidinones (linezolid)

20
Q

Give examples of nucleic acid synthesis inhibitors 🧬

A

πŸ”Ή Fluoroquinolones (ciprofloxacin, levofloxacin) – inhibit DNA gyrase/topoisomerase IV
πŸ”Ή Rifamycins (rifampicin) – inhibit RNA polymerase
πŸ”Ή Nitroimidazoles (metronidazole) – DNA strand breakage

21
Q

Give examples of antibiotics that inhibit folate synthesis 🦠

A

πŸ”Ή Sulfonamides – inhibit dihydropteroate synthase
πŸ”Ή Trimethoprim – inhibits dihydrofolate reductase
πŸ’‘ Often combined as co-trimoxazole

22
Q

Give examples of antibiotics that disrupt cell membrane integrity ⛓️‍πŸ’₯

A

πŸ”Ή Polymyxins (colistin, polymyxin B) – MDR Gram-negative, nephro/neurotoxic
πŸ”Ή Daptomycin – Gram-positive resistant, inactivated by lung surfactant

23
Q

What is MIC?

A

Minimum Inhibitory Concentration = lowest antibiotic concentration preventing visible growth. Guides dosing to ensure drug stays above MIC for efficacy.

24
Q

Time-dependent antibiotics ⏳ – definition and examples

A

Efficacy depends on time above MIC. Use prolonged/continuous infusions in ICU.
Examples: beta-lactams, vancomycin.

25
Concentration-dependent antibiotics πŸ“ˆ – definition and examples
Efficacy depends on high peak:Cmax ratio. Dose once daily to maximise peak. Examples: aminoglycosides.
26
AUC-dependent antibiotics πŸ“Š – definition and examples
Efficacy depends on total exposure (AUC:MIC). Use TDM for vancomycin (AUC:MIC >400). Examples: fluoroquinolones, vancomycin, linezolid.
27
What is antimicrobial stewardship (AMS)?
Coordinated strategies to optimise antimicrobial use: right drug, dose, route, duration, and review. Improves outcomes, reduces resistance, minimises side effects.
28
Core principles of AMS πŸ“‹
1️⃣ Right Drug – likely pathogens, site, resistance patterns 2️⃣ Right Dose – adjust for renal/hepatic function 3️⃣ Right Route – IV to PO switch when appropriate 4️⃣ Right Duration – usually 5–7 days unless indicated 5️⃣ Right Review – reassess at 48–72h
29
Four main mechanisms of antimicrobial resistance 🧬
1️⃣ Enzymatic degradation/modification (beta-lactamases, aminoglycoside enzymes) 2️⃣ Altered target site (MRSA, VRE) 3️⃣ Efflux pumps (Pseudomonas) 4️⃣ Reduced permeability (porin loss)
30
Examples of common resistant organisms in ICU πŸ₯
MRSA, VRE, ESBL Enterobacteriaceae, CRE, MDR Pseudomonas, MDR Acinetobacter, AmpC producers, C. difficile, azole-resistant Candida auris
31
Challenges of fungal infections in ICU πŸ„
Non-specific presentation, delayed diagnosis, rising incidence, limited treatment, resistance, need for source control, high mortality
32
Most common causes of invasive candidiasis 🧫
Candida albicans (most common) Others: C. glabrata, C. parapsilosis, C. tropicalis, C. auris