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Year 3 Med 1 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What are the causes of infection?

A
  • Bacteria
  • Fungi
  • Viruses
  • Parasites
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2
Q

What is bacteria and give some examples of some bacteria

A
  • Single celled organisms with phospholipid bilayer membranes
  • Only a tiny subset infect humans e.g.
    • Staphylococcus aureus
    • Escherichia coli
    • Streptococcus pneumoniae
    • Campylobacter jejuni
    • Mycobacterium tuberculosis
    • Yersinia pestis
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3
Q

What is fungi and give some examples

A
  • Fungi (type of eukaryote): Usually divided into moulds vs yeasts
  • no peptidoglycan cell wall
  • ribosomes are less distinct from our own
  • more difficult to find drug targets
  • Only a subset infect humans, eg:
    • Candida sp.
    • Aspergillus sp.
    • Dermatophytes eg Trichophyton interdigitale
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4
Q

What is a virus and give some examples

A
  • Viruses: Replicate inside living cells of a cellular organism
    • Hence, difficult to target them selectively (thus, supportive management and prevention → important)
  • All cellular organisms have viruses, including Archaea and Bacteria
  • Only a subset infect humans, eg:
    • SARS-2 coronavirus
    • Influenza virus
    • Measles virus
    • HIV, EBV, CMV, hepatitis viruses

Not included in the three-domain system because non-cellular!

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5
Q

What is a parasite and give some examples

A
  • Parasites: Loose term covering various not-closely-related, multicellular organisms eg
    • Protozoa: Plasmodium malariae, Trypanosoma brucei, amoebae
    • Helminths: tapeworms, flatworms, roundworms
    • ‘Ectoparasites’: lice, mites, fleas
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6
Q

What is the difference between antibiotics and antiseptics?

A
  • Antibiotics: Broadly, drugs that kill* pathogens *without killing people
  • Overlap between antibiotics and antiseptics, but essentially antibiotics bind to specific targets while antiseptics act more generally

Antibiotic: technically a naturally-occurring rather than a man-made antimicrobial but in practice the terms are synonymous

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7
Q

What exceptions are there to drugs that work on more than 1 group?

A
  • Exceptions:
    • Metronidazole active against flagellate parasites (‘Flagyl’) and strictly anaerobic bacteria
    • Co-trimoxazole active against bacteria and Pneumocystis jirovecii
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8
Q

How can we use antibiotics?

A
  • Treatment of infection
    • Curative – ‘course’ of varying length
    • Suppressive – often indefinitely
  • Prevention of infection
    • Before the infective event:
      • prophylaxis – usually single dose
      • eg operative prophylaxis
    • After the infective event:
      • technically ‘pre-emptive therapy’ – single dose or short course
      • eg meningococcal contact ‘prophylaxis’, bite injuries
  • Empiric therapy
    • ‘Best guess’
    • eg co-amoxiclav +/- gentamicin for suspected urosepsis
  • Targeted therapy
    • Directed against a specific organism
    • eg blood cultures growing E. coli susceptible to amoxicillin
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9
Q

What are the major groups of antibacterials?

A
  • Beta-lactams
    • penicillins (amoxicillin, flucloxacillin) → end in -cillin
    • cephalosporins (cefalexin,cefuroxime) → start with cef-
    • (monobactams → aztreonam)
    • carbapenems (imipenem, meropenem)
  • Macrolides/azalides/lincosamides
  • Tetracyclines (end in -cycline)
  • Aminoglycosides
  • Quinolones
  • Glycopeptides
  • Others:
    • trimethoprim (UTI), nitrofurantoin (UTI), fosfomycin (UTI), colistin/colomycin (last resort for Gram -ve), chloramphenicol (eyes), linezolid (allergies OR MRSA infections), metronidazole (against strict anaerobes), rifampicin (TB)
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10
Q

What do most antibacterials target?

A
  • Target one of:
    • Cell wall (peptidoglycan)
    • Protein synthesis (ribosomes)
  • A few target:
    • DNA replication
    • cell membrane
    • folate metabolism
  • Generally (not always):
    • Cell wall agents are bacteriocidal
    • Ribosomal agents are bacteriostatic
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11
Q

Draw a beta-lactam ring

A
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12
Q

Explain how beta lactams work

A
  1. Beta-lactam ring binds irreversibly to the enzymes that manufacture the bacterial peptidoglycan cell wall (‘penicillin-binding proteins’)
  2. Cell can’t make peptidoglycan
  3. Cell dies
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13
Q

Draw the anatomy of a bacterium

A
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14
Q

What is this condition?

Likely pathogens causing it?

What is the treatment & the alternative treatment?

A
  • Cellulitis
  • Likely pathogens:
    • Probably Streptococcus pyogenes
    • Possibly another pyogenic streptococcus or Staphylococcus aureus
  • Typical treatment:
    • Flucloxacillin
  • Alternatives:
    • Ceftriaxone
    • Clindamycin
    • Linezolid
    • Daptomycin
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15
Q

Explain how glycoproteins work (& example → main role)

A

E.g. vancomycin → for treating C.difficile

  • Cell wall activity:
    • molecule binds growing peptidoglycan cross-links
  • Only active against Gram positive organisms
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16
Q

Explain how macrolides work (& example → main roles)

A

E.g. erythromycin, clarithromycin (usually alternative to penicillins e.g. legionella & chlamydia trachoma’s & atypical pneumonias)

  • Bind to bacterial ribosomes
    • prevent protein synthesis > stops cell growing/dividing
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17
Q

What condition, pathogen, treatment would this patient have?

A
  • Community-acquired pneumonia
  • Likely pathogens:
    • Streptococcus pneumoniae
    • Haemophilus influenzae
    • but could be Legionella etc
  • Typical treatment:
    • co-amoxiclav plus
    • clarithromycin
18
Q

Explain how tetracyclines work and examples & main roles

A

e.g. tetracycline, doxycycline

  • Bind to bacterial ribosomes
    • prevent protein synthesis > stops cell growing/dividing
  • Good for respiratory infections, skin conditions (acne)
19
Q

Explain how aminoglycoside work and give examples & main roles

A

e.g. gentamicin

  • Given IV OR topically
  • Bind to bacterial ribosomes
    • Prevent protein synthesis > stops cell growing/dividing

Main roles

  • Not often used in isolation these days, though could do for UTI
  • Usually used in combination e.g.
    • UTI OR neutropenic sepsis
    • Streptococcal endocard itis
20
Q

Explain how quinolones work and examples & main roles

A

E.g. ciprofloxacin

How work

  • Bind to topoisomerase IV / DNA gyrase–DNA complexes
    • prevents DNA replication > stops cell growing/dividing

Main roles

  • Increasingly restricted* by side effects generally used when *no other options

well absorbed PO

21
Q

What are some antifungal drugs?

A
  • Imidazoles
  • Triazoles
  • Echinocandins
22
Q

What is this condition?

A

Thrush/Oral Candida

23
Q

What is this condition?

24
Q

Give examples of some antiviral drugs

A
  • Aciclovir
  • AZT for HIV
  • Oseltamivir for influenza
  • remdesivir for COVID-19
25
Give examples of ***antiparasitic*** drugs and what they are used for
* ***Mebendazole*** for *threadworms (in caecum → lay eggs then eggs into anus → causes itching bum → spread to others)* * ***Permethrin*** or malathion for *head lice* and *scabies*
26
Why does **antibiotic resistance** happen?
* Pathogens are living things and *evolve* in *response* to selective pressure * They become *resistant* to *antibiotics*! * There are *fewer* and *fewer* new *antibiotics* coming to market
27
What is this condition?
* **Paronychia** * With a *pustule*
28
What is the current treatment for **gonorrhoea**?
* **IM ceftriaxone**
29
What are the **mechanisms** of *acquired resistance*?
* **Bacterium destroys the antibiotic** * beta-lactamases * aminoglycoside modifying enzymes * **Bacterium modifies its target** * penicillin-binding proteins in PRP * peptidoglycan structure in VRE * ribosomal proteins in macrolide and tetracycline resistance * **Bacterium shuts the door** * reduced permeability eg ertapenem resistance in Klebsiella * **Bacterium pushes it out** * efflux pumps
30
Why is ***antimicrobial*** _resistance_ a bad thing?
1. Infections are ***_harder_*** to treat → need more *_toxic_*, more *expensive*, less convenient agents 2. Infections can be more ***severe*** 1. delayed optimisation of treatment 2. *_virulence_* often linked to resistance 3. Infections can be more ***common*** 1. failure of *prophylaxis* 2. *vicious circles* related to virulence and colonisation resistance
31
How can we **prevent** antibiotic resistance?
* *Global coalition (e.g. agriculture, new drugs)* * *Demand: reduce antibiotic use (patient education → more in PRIMARY CARE, surveillance, restrictions)* * *Supply: develop _new_ antibiotics*
32
What is **antibiotic stewardship**?
* Things we do to *_optimise_* the *treatment* of current patients *_without_* *compromising* the care of future patients * Guidelines * Better diagnostics * Prescriber education * Patient education * Use antibiotics **LESS** *(only when needed → when addvised by microbiologist)*and use them **BETTER** (*using narrower spectrum antibiotics)*
33
Explain *C.diff* and what the approaches are to minimise it?
* ***Clostridioides difficile*** infection * An *ecological side effect* of *antibiotic* use ***_Approaches_*** * Clean healthcare environment * chlorine better than detergent * Don’t give it to people * wash your hands * clean your equipment * Isolate cases * +/- carriers * Antimicrobial stewardship
34
When to do if someone says they have an ***allergy*** to ***penicillin***?
* Don’t take this at face value, always explore: * vomiting / diarrhoea / dyspepsia – intolerance *_not_* *allergy* * *_rash_* – cephalosporins *probably ok* * ***_anaphylaxis_*** – *_avoid_* all beta-lactams, use something else * ***10***% of people think they are allergic to penicillin, only ***_1_***% really are
35
What to do when someone has a UTI?
* Manage ***symptomatically*** * take a sample, wait and give *targeted treatment* * treat ***empirically*** * want to cover *E. coli* and other ‘coliforms’ * want something well absorbed PO * want something *well tolerated* and preferably *cheap*: * *nitrofurantoin* * *trimethoprim* * (refer to previous ***cultures***)
36
What are some **symptoms** of a UTI?
37
What to do when someone has **bronchitis**?
* Manage ***symptomatically*** * take a *sample*, wait and give *targeted* *treatment* * treat ***empirically*** * want to cover *Haemophilus influenza, Streptococcus pneumonia and Moraxella catarrhalis* * want something well absorbed PO * want something *well tolerated* and preferably *cheap*: * *doxycycline* * *amoxicillin* * *clarithromycin*
38
What to do if someone has a ***skin infection*** like this:
* Manage ***symptomatically*** * take a sample, wait and give targeted treatment * treat ***empirically*** * want to cover *Staph aureus*, streptococci * want something well absorbed PO * want something *well tolerated* and preferably *cheap* * *flucloxacillin* * *doxycycline* * *clarithromycin*
39
What to do if someone has **endocarditis**?
* Manage symptomatically (rare, will have *night sweats non-specific symptoms as bacteria from the valves breaks off and gets into the blood stream)* * take a sample, wait and give targeted treatment * treat ***empirically*** * want to cover alpha-haemolytic streptococci * in some scenarios want to cover staphylococci and enterococci * need something bacteriocidal and available IV * high dose ***amoxicillin*** plus ***gentamicin*** * *vancomycin plus gentamicin*
40
What to do if someone has **bacterial meningitis**?
* Manage ***symptomatically*** * ***DO A LUMBAR FUNCTURE*** * take a sample, wait and give *targeted treatment* * treat ***empirically*** * want to cover *Neisseria meningitidis*, *Streptococcus pneumoniae* +/- *Listeria monocytogenes (when pregnant/immunocompromised)* * need something IV, which crosses BBB and bacteriodical * typically *cefotaxime +/- amoxicillin*

Year 3 Med 1 (19 decks)

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