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Clinical Pharmacology And Therapeutics > Infections > Flashcards

Infections Flashcards

1
Q

What are some problems surrounding discovery of new antibiotics

A
  • cost - not beneficial to drug companies
  • rapid resistance
  • time consuming
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2
Q

Potential solutions to antibiotic resistance

A

Improve diagnostics

Stewardship

Novel targets - bacteriophages (viruses that can infect bacteria or gene targets)

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3
Q

What are gram +ve bacteria

A

Thicker peptidoglycan layer - stain purple

G+ cocci in clusters (rounder shape) - staphylococci

G+ diplococci - streptococcus pneumoniae or enterococcus

G+ cocci in chains = streptococci

G+ bacilli - aerobic = listeria, anaerobic = clostridium

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4
Q

What are gran -ve bacteria

A

G- diplococci - neisseria (gonorrhoea)

G- bacilli - enterobacterales eg E. coli
Pseudomonas
Anaerobe: bacteroides

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5
Q

What kinds of antibiotics act on the cell wall of the bacteria

A

Beta lactams:
- penicillins
- cephalosporins
- carbapenems
- monobactams

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6
Q

What types of anti bacterial act on the cell membrane

A

Polymysins

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7
Q

What types of antibiotics act on the protein synthesis of the bacteria (ribosome pathways)

A

30S subunit:
- tetracyclines
- aminoglycosides

50S subunits: (forming peptide bonds)
- macrolides
- clindamycin
- linezolid
- chloramphenicol
- streptogramins

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8
Q

What types of anitbitoics act on the folate synthesis in bacteria

A

Sulfonamides
Trimethoprim

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9
Q

What types of antibiotics act on the DNA gyrase in nucleic acid synthesis

A

Quinolones

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10
Q

What types of antibiotics act on the RNA polymerase in nucleic acid synthesis

A

Rifampin

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11
Q

Describe the structure of beta lactam antibiotics (penicillins)

A

Beta lactam ring

5 membered thiozolidine ring (3C, 1S, 1N)

Side chain - determines spectrum and pharmacological properties

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12
Q

Describe the structure of beta lactam antibiotics (cephalosporins)

A

Beta lactam ring

6 membered dihydrothiazine ring (4C, 1S, 1N)

Modification of 6 C ring gives different cephalosporins

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13
Q

Describe the structure of beta lactam antibiotics (carbapenems)

A

Beta lactam ring

5 membered ring (4C, 1N)

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14
Q

Describe the mode of action of beta lactam antibiotics

A

Bind to and inhibit penicillin binding proteins (PBPs)

PBPs play a role in cross linking the peptidoglycan layer of cell wall

If this process is weakened it inhibits and ruptures the cell wall of the bacteria

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15
Q

What are beta lactamase inhibitors

A

Beta lactamase are a Bacterial enzyme that destroys beta lactam rings
Beta lactamase inhibitors:
- weaken antibacterial activity
- are given in combination with B-lactam antibiotics
- resemble the B-lactam antibiotics in structure
- bind to B-lactamase -> protect B-lactam from destruction

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16
Q

What are some examples of B-lactamase inhibitors

A

Clavulanic acid - combined with amoxicillin = co-amoxiclav

Tazobactam - combined with penicillin - tazocin

Sulbactam - combined with ampicillin = ampicillin- sulbactam

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17
Q

What are glycopeptide antibiotics

A

Act on cell wall of bacteria
Eg vancomycin, teicoplanin.
Broad G+ cover, lack G- cover

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18
Q

What are the groups of fungus

A

Yeasts - single celled - reproduce by budding

Moulds - multicellular - grow by branching

Dimorphic- moulds at room temp, yeasts at body temp ( not seen commonly in UK)

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19
Q

What are some examples of anti fungal drugs

A

Azoles: triazoles eg fluconazole, voriconazole - used more in hosp
Imidazoles eg clotrimazole, miconazole - mainly topical

Polyenes: amphotericin B - covers most infections
Nystatin - topical for thrush

Echinocandins: caspofungin and anidulafungin - candidaemias

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20
Q

Describe the structure and use of anti fungal drugs

A

Triazoles eg fluconazole can act on dematophytes, candida, cryptococcus - some act on moulds and dimorphic fungi

Polyenes - eg amphotericin B- ampisomal form reduces toxicity treats most systemic mycoses

Echinocandins - anidulafungin - used mostly for candidaemias

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21
Q

Define chemoprophylaxis

A

Use of an anti microbial drug to prevent an infection
Distinct from immunisation

Eg use of anti malarial drugs to prevent malaria in travellers from the UK visiting malaria endemic countries

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22
Q

Describe an example of chemoprophylactic treatment

A

IV cerufoxime and metronidazole started at the time of surgery for faecal peritonitis secondary to a perforated colonic carcinoma

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23
Q

How can chemoprophylaxis be thought of as antibiotic abuse

A

Unnecessary use of anti microbial drugs as chemoprophylactic agents eg not a significant risk of infection or not serious consequences of infection

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24
Q

What factors mean you should consider chemoprophylaxis

A
  • significant and predictable risk of infection
  • serious consequences of infection
  • period of highest risk can be ascertained
  • microbial causes of infection are predictable
  • antimicrobial sensitivity of the infections are predictable
  • cheap and reasonably safe antimicrobial agents available
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25
Q

Explain some examples of disadvantages of chemoprophylaxis

A
  • cost
  • adverse effects
  • disturbance of normal human bacterial flora - increases risk of antibiotic resistant bacteria growing in gut and also increases risk of C.diff
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26
Q

Give an example of inappropriate chemoprophylaxis

A

Long term antibiotics to prevent UTI in patients with in dwelling urinary catheters (inappropriate as you can’t predict which pathogens are going to infect)

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27
Q

Describe chemoprophylactic treatment for malaria

A

Variety of regimens
- chloroquine +/- proguanil
- mefloquine
- doxycycline, atovaquone (malarone = proguanil + ataovaquone)

Continued for 4 weeks after leaving malarious area, except Malarone which is 1 week

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28
Q

Explain prophylaxis for invasive group A strep infections

A

Penicillin PO given to close contacts of patient with group A strep infections : alternative erythromycin or azithromycin

Prophylaxis for both mother and baby recommended if either develops invasive group A strep infection in neonatal period

Prophylaxis for all household if 2 or more cases of invasive group A strep disease in 30 days

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29
Q

What is group B strep

A

Part of normal vaginal flora
Can cause neonatal meningitis and septicaemia
Particular risk for pre term, low birth weight infants

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30
Q

When is penicillin or clindamycin prophylaxis given during labour

A
  • pre term labour
  • prolonged rupture of membranes
  • history of previous strep B neonatal infection in previous pregnancy
  • mother known to be carrying group B strep in this pregnancy
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31
Q

What is rheumatic fever

A

Immunological response to infection with strep A
Rare in UK but has re-appeared over past 20 years
2-3 weeks post infection - carditis leading to heart valve damage, joint inflammation, rashes, chorea
Prone to repeated attacks - progressive valvular damage

After 1 attack of rheumatic fever: penicillin prophylaxis 250mg bd until at least 16 years old to prevent recurrence

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32
Q

Describe chemoprophylaxis in bacterial meningitis and meningococcal disease

A

Chemoprophylaxis for close contact: kissing, mouth to mouth resuscitation or those living in the same household

  • rifampicin 600mg PO bd for 2 days (makes contraceptive pill ineffective and turns contact lens orange)
  • ciprofloxacin 500mg PO stat
  • ceftriaxon: IM for pregnant contacts as others are contraindicated
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33
Q

Chemoprophylaxis of bacterial meningitis (Hib)

A

Rare in UK due to immunisation

Prophylaxis for all household contacts if child <4 lives in house
- rifampicin 600mg PO od 4 days

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34
Q

Describe risk of infection in splenectomised patients

A

Severe overwhelming infections
- capsulated bacteria
* streptococcus pneumoniae
* meningococcal, Hib

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35
Q

Describe prophylaxis in splenectomised patients

A

Prophylaxis with penicillin to prevent pneumococcal infections (also used for children with sickle cell disease)
- proven benefit in children, unclear in adults
- compliance issue
- highest risk in first 2 years following splenectomy
- superinfection with resistant bugs

36
Q

Examples of conditions that cause immunosuppression

A
  • HIV
  • malignancy of immune system
  • cancer chemotherapy
  • steroids, azathioprine
  • solid organ transplants, bone marrow transplants
37
Q

Examples of prophylaxis in HIV

A

Co-trimoxazole to prevent recurrent PCP (pneumocystis) following 1st infection of when CD4 count <200

38
Q

Prophylaxis in bone marrow transplant

A

Aciclovir to prevent herpes
Fluconazole to prevent candida

39
Q

How to treat infections following trauma / bites

A
  1. Surgical debridement (clean)
  2. Delayed surgical closure (dont suture as need to get bacteria out)
    Co-amoxiclav, metronidazole
    Doxycycline
    Tetanus booster +/- tetanus immunoglobulin
40
Q

What prophylaxis is given to prevent endocarditis (controversial)

A

Antibiotic prophylaxis no longer recommended in BNF (UK)

High risk patients = prosthetic heart valve, previous endocarditis are given antibiotic prophylaxis in US but not UK

41
Q

What are the 4 types of surgical operation

A
  1. Clean: hernia repair, mastectomy - antibiotic prophylaxis not needed
  2. Clean with implant eg mastectomy with breast implant, aortic aneurysm repair, hip replacement, heart valve replacement: antibiotic prophylaxis indicated to prevent infection of skin organisms of low pathogenicity
  3. Contaminated: antibiotic prophylaxis indicated as predictable risk eg elective colorectal surgery
  4. Dirty: antibiotic prophylaxis not indicated requires full therapeutic course of antibiotics eg emergency colorectal surgery in peritonitis. 5-7 day course of broad spectrum antibiotics (IV cefuroxime and metronidazole)
42
Q

What are some common faults with surgical antibiotic prophylaxis

A
  1. Used for clean operations
  2. Given for too long
  3. Often given without regard to previous microbiology reports or recent antibiotic treatment as you can’t give the same prophylaxis twice in a short space of time as the flora will have been altered
43
Q

Describe post exposure prophylaxis for HIV

A

Considered for
- penetrating needle stick injuries
- blood splashes to mucous membranes or non intact skin
- sexual contact (rape)
- when source is known or strongly suspected to be HIV +ve

PEP ideally given within 1 hour but offered up to 2 weeks after exposure
Combination of anti-retroviral drugs
AZT, DDI + protease inhibitors
Take for 4 weeks

44
Q

Describe the burden of hospital acquired infections

A
  • increased length of stay
  • increased costs
  • increased morbidity and mortality
  • affects 6% of patients
45
Q

What is the difference between colonisation and infection

A

Colonisation is the established presence and multiplication of bacteria without damage / invasoin eg coagulase negative staphylococcus on skin surface - doesn’t need to be treated with antibiotics

Infection is the entry and multiplication in tissues and causing damage eg S. aureus wound infection

Some bacteria are almost always colonisers and rarely pathogens and some are usually pathogens

46
Q

Define a carrier

A

A person who harbours microbes with no signs of disease

47
Q

What are microbial reservoirs

A

Anywhere where organisms can live and replicate
Eg mosquito infested swamp where mosquito scarring P. Vivas replicate inside mosquito and pass to offspring

Eg humans such as N. Meningitidis

48
Q

Describe the chain of infection

A

Start with a source
Some means of transmission spreading microorganisms
Host - vulnerable to being colonised and / or infected
Carriage state - may or may not be symptomatic
Contamination of environment, establishment of new reservoir eg someone with c.diff using a commode

49
Q

What are exogenous sources of infection

A

Exogenous - from another person or environment:
- airborne (legionnaire’s disease, TB, respiratory viruses)
- contact (salmonella, staphylococcus)
- inoculated (HIV or hepatitis from needle stick injury, malaria from mosquito bite, tetanus)

50
Q

What are endogenous sources of infection

A

Self infection with own organisms
Eg surgical wound infections, pneumonia, UTI

51
Q

Why is infection control more challenging in hospitals

A

High antibiotic use - more resistant bacteria around
Medical devices - IV lines, catheters, ventilation, peritoneal dialysis, surgical drains and wounds
Environment - crowding, patient movement, lack of isolation facilities
Frail, elderly, susceptible people

52
Q

Define HCAI

A

Health care associated infection (HCAI)
- occurs more than 48 hours after admission to hospital
- occurs within 10 days of discharge from hospital (30 days for surgical wound)
- occurs within 72 hours of an outpatient procedure

53
Q

Describe ways of reducing patient susceptibility

A

Immunity: vaccinate, prophylaxis, isolate
Devices: remove if infected, remove if not needed, avoid unnecessary insertion
Antibiotic: reduce exposure, target therapy

54
Q

What is the difference between ADRS and side effects

A

ADRs are always disadvantageous

55
Q

What is a type A augmented response

A

The normal pharmacological response is undesirable
Usually reduce dosage to reduce adverse events

56
Q

What is C. difficile

A

Gram +ve anaerobic bacteria
Antibiotics can disrupt the bowel flora allowing colonisation of c. Diff (acquired following germination of ingested spores)
Antibiotics = kills other gut bacteria and allows C.diff to proliferate
This can cause diarrhoea or pseudomembranous colitis

57
Q

Give examples of C diff associated diarrhoea antibiotics

A

Cephalosporins
Clindamycin (mainly used in bone infections)
Quinolones

58
Q

Why are you likely to be allergic to all the penicillins if allergic to one

A

Because of the common beta lactam structure

59
Q

What is a beta- lactam allergy

A
  • penicillin / cephalosporins / carbapenems / monobactams
    GI upset is common
    Rash = no more penicillins but other B-lactams are probably ok (risk of cross over allergy is low)
    Angioedema / anaphylaxis = no more B - lactams; use other class of agent
60
Q

Give some examples of skin reactions as ADRs

A

Uritcaria (raised itchy rash)
Erythematous eruptions: reddening (maculopapular)
Toxic epidermal necrolysis: rare but often fatal with blistering and skin peels off (sulphonamides)
Steven Johnson syndrome: serious blistering reaction on face (beta lactams, can be caused by drugs other than antibacterials)

61
Q

Define drug interaction

A

When the effects of one drug are changed by the presence of another drug, food, drink or an environmental change

62
Q

What is CYP-mediated metabolism

A

Many drugs are metabolised by multiple CYPs
Some drugs metabolised by single CYP- these are most likely to be involved in clinically relevant interactions (more vulnerable)

63
Q

What is enzyme induction

A

Increase activity of metabolising enzymes eg rifampicin
Reduces plasma conc of a range of drugs eg rifampicin increases metabolism of OCs

64
Q

How to calculate the therapeutic range

A

[toxic concentration] - [therapeutic concentration]

Defines the window between toxic and therapeutic drug concentrations eg wide for penicillin and narrow for gentamicin

65
Q

Why is chloramphenicol rarely used PO

A

High risk of aplastic anaemia (bone marrow toxicity)

66
Q

Describe 5 basic principles of antibiotic use

A
  1. Administer an antibiotic that provides a level sufficient to inhibit or kill the infecting organism
  2. Continue treatment until the host is able to complete the curing and healing process
  3. Drain infections of close spaces if necessary
  4. Know what responses to expect
  5. Be prepared to re-evaluate if this response is not observed
67
Q

What are the principles of rational antimicrobial use

A
  1. Ensure effective treatment of patients with infections
  2. Minimise collateral damage from antimicrobial use
    - increased selection of resistant organisms
    - antibiotic treatment related illnesses eg c.diff
    - increased risk of adverse effects
    - increased cost
68
Q

How to know when it is safe to switch a patient from IV antibiotics to oral (COMS)

A

Clinical improvement observed
Oral route is not compromised
Markers are showing trend towards normalising
Specific indication / deep seated infection

69
Q

Possible causes of antibiotic treatment failure

A
  1. Wrong diagnosis
  2. Wrong choice of antibiotic
  3. Inadequate duration
  4. Inadequate dose
  5. Antibiotic given by wrong route
  6. New problem or secondary infection
  7. Compliance
  8. Drug resistance developed during treatment
  9. Pus requiring drainage or foreign body needs removing
70
Q

MOA of macrolides eg clarithromycin

A

Prevention of translocation of bacterial 50s ribosome subunit along the mRNA

71
Q

MOA of tetracycline

A

Binding to bacterial 30S ribosome and prevent tRNA from binding

72
Q

MOA of cephalosporins

A

Inhibition of bacterial cell wall transpeptidases

73
Q

MOA of quinolones eg ciprofloxacin

A

Inhibition of bacterial DNA gyrases

74
Q

MOA of trimethoprim

A

Inhibition of bacterial dihydrofolate reductase

75
Q

MOA of sulphonamides

A

Inhibition of bacterial dihydropteroate synthase

76
Q

What is often combined with amoxicillin to reduce the effects of beta lactamases (a beta lactamase inhibitor)

A

Clavulanic acid

77
Q

MOA of vancomycin (a glycopeptide)

A

Inhibiton of growth of peptidoglycan chain

78
Q

If a patient has an amoxicillin allergy which causes a hypersensitivity reaction what is the best antibiotic to prescribe alternatively

A

Macrolide as a penicillin allergy applies to all penicillins and has some cross reactivity with cephalosporins

79
Q

What is use of macrolides complicated with

A

Drug interactions through inhibition of drug metabolism (CytP450 inhibition)

80
Q

Which 2 antibacterial agents interfere with bacterial wall synthesis

A

Vancomycin (glycopeptide)
Amoxicillin (penicillin)

81
Q

Which class of antibacterial agents directly inhibits bacterial protein synthesis

A

Macrolides eg clarithromycin as they block protein synthesis at the level of the bacterial ribosome

82
Q

Which antibacterial agent interferes with purine and pyrimidine synthesis

A

Trimethoprim

83
Q

What are 2 important adverse effects of the aminoglycoside gentamicin

A

Ototoxicity
Nephrotoxicity

84
Q

How does an eGFR of 30 affect a gentamicin regimen

A

Increases the plasma half life

85
Q

What is an important adverse effect of quinolones eg ciprofloxacin

A

Tendon damage

Clinical Pharmacology And Therapeutics (7 decks)

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