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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
Explain some examples of disadvantages of chemoprophylaxis
- 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
26
Give an example of inappropriate chemoprophylaxis
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)
27
Describe chemoprophylactic treatment for malaria
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
28
Explain prophylaxis for invasive group A strep infections
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
29
What is group B strep
Part of normal vaginal flora Can cause neonatal meningitis and septicaemia Particular risk for pre term, low birth weight infants
30
When is penicillin or clindamycin prophylaxis given during labour
- 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
31
What is rheumatic fever
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
32
Describe chemoprophylaxis in bacterial meningitis and meningococcal disease
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
33
Chemoprophylaxis of bacterial meningitis (Hib)
Rare in UK due to immunisation Prophylaxis for all household contacts if child <4 lives in house - rifampicin 600mg PO od 4 days
34
Describe risk of infection in splenectomised patients
Severe overwhelming infections - capsulated bacteria * streptococcus pneumoniae * meningococcal, Hib
35
Describe prophylaxis in splenectomised patients
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
Examples of conditions that cause immunosuppression
- HIV - malignancy of immune system - cancer chemotherapy - steroids, azathioprine - solid organ transplants, bone marrow transplants
37
Examples of prophylaxis in HIV
Co-trimoxazole to prevent recurrent PCP (pneumocystis) following 1st infection of when CD4 count <200
38
Prophylaxis in bone marrow transplant
Aciclovir to prevent herpes Fluconazole to prevent candida
39
How to treat infections following trauma / bites
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
What prophylaxis is given to prevent endocarditis (controversial)
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
What are the 4 types of surgical operation
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
What are some common faults with surgical antibiotic prophylaxis
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
Describe post exposure prophylaxis for HIV
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
Describe the burden of hospital acquired infections
- increased length of stay - increased costs - increased morbidity and mortality - affects 6% of patients
45
What is the difference between colonisation and infection
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
Define a carrier
A person who harbours microbes with no signs of disease
47
What are microbial reservoirs
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
Describe the chain of infection
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
What are exogenous sources of infection
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
What are endogenous sources of infection
Self infection with own organisms Eg surgical wound infections, pneumonia, UTI
51
Why is infection control more challenging in hospitals
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
Define HCAI
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
Describe ways of reducing patient susceptibility
Immunity: vaccinate, prophylaxis, isolate Devices: remove if infected, remove if not needed, avoid unnecessary insertion Antibiotic: reduce exposure, target therapy
54
What is the difference between ADRS and side effects
ADRs are always disadvantageous
55
What is a type A augmented response
The normal pharmacological response is undesirable Usually reduce dosage to reduce adverse events
56
What is C. difficile
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
Give examples of C diff associated diarrhoea antibiotics
Cephalosporins Clindamycin (mainly used in bone infections) Quinolones
58
Why are you likely to be allergic to all the penicillins if allergic to one
Because of the common beta lactam structure
59
What is a beta- lactam allergy
- 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
Give some examples of skin reactions as ADRs
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
Define drug interaction
When the effects of one drug are changed by the presence of another drug, food, drink or an environmental change
62
What is CYP-mediated metabolism
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
What is enzyme induction
Increase activity of metabolising enzymes eg rifampicin Reduces plasma conc of a range of drugs eg rifampicin increases metabolism of OCs
64
How to calculate the therapeutic range
[toxic concentration] - [therapeutic concentration] Defines the window between toxic and therapeutic drug concentrations eg wide for penicillin and narrow for gentamicin
65
Why is chloramphenicol rarely used PO
High risk of aplastic anaemia (bone marrow toxicity)
66
Describe 5 basic principles of antibiotic use
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
What are the principles of rational antimicrobial use
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
How to know when it is safe to switch a patient from IV antibiotics to oral (COMS)
Clinical improvement observed Oral route is not compromised Markers are showing trend towards normalising Specific indication / deep seated infection
69
Possible causes of antibiotic treatment failure
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
MOA of macrolides eg clarithromycin
Prevention of translocation of bacterial 50s ribosome subunit along the mRNA
71
MOA of tetracycline
Binding to bacterial 30S ribosome and prevent tRNA from binding
72
MOA of cephalosporins
Inhibition of bacterial cell wall transpeptidases
73
MOA of quinolones eg ciprofloxacin
Inhibition of bacterial DNA gyrases
74
MOA of trimethoprim
Inhibition of bacterial dihydrofolate reductase
75
MOA of sulphonamides
Inhibition of bacterial dihydropteroate synthase
76
What is often combined with amoxicillin to reduce the effects of beta lactamases (a beta lactamase inhibitor)
Clavulanic acid
77
MOA of vancomycin (a glycopeptide)
Inhibiton of growth of peptidoglycan chain
78
If a patient has an amoxicillin allergy which causes a hypersensitivity reaction what is the best antibiotic to prescribe alternatively
Macrolide as a penicillin allergy applies to all penicillins and has some cross reactivity with cephalosporins
79
What is use of macrolides complicated with
Drug interactions through inhibition of drug metabolism (CytP450 inhibition)
80
Which 2 antibacterial agents interfere with bacterial wall synthesis
Vancomycin (glycopeptide) Amoxicillin (penicillin)
81
Which class of antibacterial agents directly inhibits bacterial protein synthesis
Macrolides eg clarithromycin as they block protein synthesis at the level of the bacterial ribosome
82
Which antibacterial agent interferes with purine and pyrimidine synthesis
Trimethoprim
83
What are 2 important adverse effects of the aminoglycoside gentamicin
Ototoxicity Nephrotoxicity
84
How does an eGFR of 30 affect a gentamicin regimen
Increases the plasma half life
85
What is an important adverse effect of quinolones eg ciprofloxacin
Tendon damage

Clinical Pharmacology And Therapeutics (7 decks)

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