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MPharm2 SL22105 > Treatment of infection > Flashcards

Treatment of infection Flashcards

Antibacterial MOA antibacterial MOR Clinical antibiotics 1-5 Prophylaxis Stewardship Antifungals Antibiotic chem 1+2 Antivirals 1+2

1
Q

What are the 2 most common cell wall synthesis inhibitors?

A

b-lactams and glycopeptides

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2
Q

What are the 4 b-lactams?

A

Penicillins, cephalosporins, carbapenems, monobactams

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3
Q

What are the 2 glycopeptides?

A

Vancomycin, teicoplanin

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4
Q

What are the three modes of action of b-lactams?

A
  1. Bind and inhibit action of Penicillin Binding Proteins
  2. Get incorporated into peptide side chain
  3. Stimulate autolysins → break down cell wall → cell lysis
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5
Q

Do b-lactams work on gram -ve or +ve?

A

Both, but more commonly on gram +ve as they have to work harder to get through the outer layer of gram -ve bacteria

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6
Q

How do glycopeptides work?

A

It binds to the terminal amino acids (d-ala – d-ala) on the peptide side chain of the monomer.

  1. Prevents X-linking of peptide side chains
  2. Prevents glycosylase enzyme from adding PG monomer onto PG chain
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7
Q

Do glycopeptides work on gram -ve or +ve?

A

gram +ve only

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8
Q

Which 2 inhibitors work on cell membranes?

A
  • polymyxins
  • lipopetides
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9
Q

How do polymyxins work?

A

Binds to Lipid A, distorts the membrane, penetrates cell wall, also allows leakage of cytoplasmic contents

Only acts on gram -ve bacteria, reserved for serious infections

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10
Q

What are the 4 modes of action that antibacterials have for nucleic acid?

A
  • metabolic inhibitors of NA synthesis (sulphonamides, trimethoprim)
  • inhibit DNA replication (fluoroquinolones)
  • affect RNA polymerase (rifamycins)
  • affect DNA (nitromidazoles)
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11
Q

What do fluroquinolones do?

A

Inhibit DNA replication
They bind to the enzyme-DNA complex, DNA gyrase removes DNA supercoils ahead of replication fork

This inhibits DNA replication and packaging of DNA within the bacterial cell → bacterial cell lysis

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12
Q

What do tetracyclines do?

A

Inhibits bacterial growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. Bacteriostatic

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13
Q

What do aminoglycosides do?

A

Bind irreversibly to the aminoacyl site of 16S rRNA of the 30S ribosomal subunit, leading to misreading of the genetic code, inhibition of translocation (tRNA binding) and increased membrane permeability

Bactericidal

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14
Q

Which 5 factors promote resistance?

A
  • Over/improper use
  • Overprescribing
  • Aging population
  • Use in farming
  • Lack of development of new classes of drug.
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15
Q

What are the 4 signs of systemic infection?

A
  • delirium
  • fever
  • raised heart rate
  • malaise
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16
Q

What is the FeverPAIN criteria?

A

(for strep throat)
Fever
Purulence (pharyngeal/tonsillar exudate)
Attend rapidly (within 3d from onset)
Inflamed tonsils
No cough or coryza

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17
Q

What are the 6 symptoms of epiglottitis?

A
  • Severe and acute onset of sore throat
  • Fever
  • Muffled voice
  • Drooling
  • Stridor
  • Tend to lean forward, breathing carefully.
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18
Q

What are the warning signs for sepsis in adults?

A

Slurred speech
Extreme shivering
Passing no urine
Severe breathlessness
It feels like you are going to die
Skin mottled

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19
Q

What are the 5 warning signs for sepsis in children?

A
  • Breathlessness
  • Non-blanching rash
  • Abnormally cold
  • Skin mottled, blue or pale
  • Convulsing
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20
Q

What is the difference between meningitis and meningococcal disease

A

Bacterial meningitis: bacterial infection of the meninges
Meningococcal disease: infection with Neisseria meningitidis.

Strongly suspect bacterial meningitis with any of fever, headache, neck stiffness, altered consciousness.

Strongly suspect meningococcal disease with any of haemorrhagic, non-blanching rash, rapidly progressive/spreading non-blanching rash, any symptoms or signs of bacterial meningitis with a non-blanching rash.

But do not rule out the other

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21
Q

What is directed therapy?

A

Culture positive, identification, sensitivities

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22
Q

What are the 4 pros of directed therapy?

A
  • we know what is causing it
  • we know about resistance
  • treatment more likely to succeed
  • can use narrower specturm antibiotics
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23
Q

What are the 3 cons of directed therapy?

A
  • We might still be wrong: could be contaminant or colonisation
  • There might be mixed cause, all organisms might not have grown
  • Some tests take time
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24
Q

What are 3 the pros of empirical therapy?

A
  • Can start therapy quickly
  • Should be effective in most cases
  • Evidence-based
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25
Q

What are the 4 cons of empirical therapy?

A
  • May sometimes be wrong
  • Causative organism might be resistant
  • Tends to be broader spectrum
  • Giving antibiotics may reduce probability of a successful culture
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26
Q

Why is infective endocarditis to difficult to eradicate?

A
  • endocardium poorly vascularised
  • bacteria buried in “vegetations”
  • slow-growing pathogens display
    antimicrobial tolerance
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27
Q

What is the first line treatment for a UTI?

A

Nitrofurantoin 100mg MR BD for three days

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28
Q

What 4 things must be considered when choosing an antibiotic?

A
  • severity of symptoms
  • risk of complications
  • local antimicrobial resistance data
  • recent antibiotic use
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29
Q

Which 3 things can affect choice of antibiotic when patient has renal impairment?

A
  • increased risk of infection
  • some drugs will be less effective
  • excretion may be impacted
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30
Q

Which 2 things can affect choice of antibiotic when patient has hepatic impairment?

A
  • increased risk of infection
  • can affect absorption distribution and clearance of drug
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31
Q

What are the 3 times it is appropriate to use IV antibiotics?

A
  • Severe life-threatening infections (e.g. sepsis, meningitis)
  • Needed for patients who are unable to take or absorb oral drugs (e.g. vomiting)
  • Prolonged iv used for ‘deep-seated’ infections (infections of bones and joints, infective endocarditis)
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32
Q

Why do some drugs need to be monitored?

A
  • Narrow therapeutic index – need to ensure antibacterial is effective while preventing toxicity.
  • These drugs can only be used in settings with facilities to monitor levels and interpret the results.
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33
Q

What are the 5 common side effects of antibiotics?

A
  • Disrupted microbiome
  • Hypersensitivity
  • Red man syndrome
  • Neurotoxicity and nephrotoxicity
  • Bone marrow disorders
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34
Q

What is a superficial surgical site infection?

A

Occurs within 30 days postoperatively and involves skin or subcutaneous tissue of the incision and at least one of the following:
- pus
- positive culture
- signs of infection

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35
Q

What is a deep incisional SSI?

A

Occurs within 30 days after the op if no implant, or within one year if implant in place and the infection appears to involve deep soft tissuesof the incision, and the patient has at least one of the following:
- pus
- positive culture
- signs of infection

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36
Q

What is an organ/space SSI?

A

Involves any part of the inner body, that is manipulated during the op. Organ/space SSI must meet the following criteria:
- Infection occurs within 30 days after the op if no implant or within 1 year if implant in place and the infection appears to be related
- Infection involves any part of the inner body that is manipulated during the op, and
- The patient has at least one of the following:
- pus
- positive culture
- signs of infection

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37
Q

What are the four degrees of contamination?

A
  • Clean - no inflammation, aseptic
  • Clean-contaminated - respiratory, alimentary or genitourinary systems entered but no leak
  • Contaminated - acute inflammation or visible contamination
  • Dirty - pus or hollow injuries
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38
Q

Which two commonly recurring infections are given prophylaxis for?

A

UTI and infective endocarditis

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39
Q

Which 3 conditions require those exposed to infected to be given prophylaxis?

A
  • Meningitis
  • HIV (after possible exposure)
  • Influenza
40
Q

What is Asplenia?

A
  • No spleen or not working
  • Prophylaxis will be required
  • Higher risk of serious infections
  • May require additional vaccinations
41
Q

What is C. diff?

A
  • Opportunistic infection
  • Overgrowth of anaerobic bacteria in the bowel
  • Associated with previous antibiotic administration
  • Faecal–oral transmission from spore contact
  • Associated colitis and diarrhoea
  • Mortality and morbidity worse in elderly
42
Q

What is FMT?

A

Faecal Microbiota Transplantation
FMT is recommended as an option to treatrecurrentC diffinfection in adults who have had 2 or more previous confirmed episodes.

Aims to restore a healthy gut microbiome.

It involves transferring intestinal bacteria and other microorganisms from healthy donor faeces into the gut of the recipient.

43
Q

Which 6 bacteria are most concerning regarding resistance?

A
  • MRSA
  • GRSA
  • VRE
  • EBSLs
  • Super gonnorhoea
  • MDR TB
44
Q

What are the 6 Rs for vaccination?

A
  • Reassurance
  • Reasons
  • Relief
  • Realistic
  • Reinforce
  • Rescue
45
Q

What is Aspergillosis?

A

Aspergillus infection in lungs

46
Q

What is Asperfilloma?

A

Fungal ball developed in lung cavity

47
Q

What are the 6 risk factors for invasive fungal infections?

A
  • Chemotherapy
  • Transplant
  • AIDS/HIV
  • Broad spectrum antibiotics
  • Indwelling catheter, in particular central IV line
  • Respiratory diseases, e.g. cystic fibrosis, Covid-19
48
Q

How are invasive fungal infections diagnosed?

A

Clinical diagnosis: medical history, symptoms, and risk factors

Cultures of blood, respiratory, or biopsy samples. Slow and not very sensitive; some species unculturable.

Direct microscopy of clinical samples
- poor sensitivity, requires expertise in fungal identification

Imaging: X-ray/CT

49
Q

What are the four categories of antifungals?

A

Azoles

Echinocandins

Polyenes

Nucleoside analogues

50
Q

What are triazoles?

A

Azoles

Mechanism of action
- Decreased ergosterol production through inhibition of fungal cytochrome p450 enzymes

Most are fungistatic
Orally active

Side effects
- Liver toxicity
- QT prolongation

Interactions
- Many drugs that affect cytochrome p450 enzymes

51
Q

What is amphotericin?

A

Antifungal (polyenes)
MoA
- Interacts directly with ergosterol, creating pores in the membrane

Broad spectrum - active against most fungi
Not orally absorbed
For severe systemic infections only

Significant side effects – toxicity is limiting factor

52
Q

What are echinocandidins?

A

Antifungal
MoA
- Inhibit 1,3-β-glucan synthase

Very poor oral bioavailability; IV only
Toxicity low, and minimal drug interactions

53
Q

What are the three mechanisms of antibiotic resistance to beta-lactams?

A
  • inactivate drug
  • alter drug site
  • alter drug uptake
54
Q

What are beta lactamases?

A

An enzyme that can deactivate beta lactam antibiotics by breaking open this beta lactam ring.

55
Q

What are beta lactamase inhibitors?

A

Chemicals added to antimicrobial treatments to prevent inactivation of beta lactam ring

56
Q

What are PBPs and how do they alter antibiotic effectivity?

A
  • PBP (penicillin binding protein) on outer membrane is the target of beta lactams
  • Mutations in the PBP can prevent binding
57
Q

What is the MoR to vancomycin?

A

altered target site

58
Q

What is the MoR to aminoglycosides?

A

drug inactivation

59
Q

What is the MoR to fluroquinolones?

A

altered target

60
Q

What is the MoR to tetracyclines?

A

efflux pumps

61
Q

What is the MoR for MDR?

A

multi-drug efflux pumps

62
Q

What are the 4 classes of beta lactamases?

A

Class A – penicillinases
Class B – metallo-β-lactamases
Class C – Cephalosporinases
Class D – ESBLs

63
Q

What are cephalosporin and cephamycin antibiotics?

A

Cephalosporins and cephamycins are alternative β-lactam antibiotics.
They bind to “Penicillin-Binding Proteins” (PBPs).
They are often used in patients where infections are resistant to penicillins.

64
Q

What are semi-synthetic cephem antibiotics?

A

Semi-synthetic cephalosporins and cephamycins can also made by using an acylase to remove the side-chain to give the cephem core.
Chemical acylation gives ‘semi-synthetic’ cephalosporins and cephamycins.

65
Q

What are the 3 strategies for overcoming beta-lactamases?

A
  • Change the structure of the antibiotic
    This is often a temporary solution due to the rapid development of resistance.
    Changing the structure of the antibiotic can substantially change the organisms against which the antibiotic is effective.
  • Co-administer a blocking antibiotic:
    The level of protection can be poor and can result in resistance to multiple antibiotics, but sometimes successful e.g., co-fluampicil
  • Use a suicide inhibitor with the antibiotic e.g., clavulanic acid:
    Inhibitors undergo catalysis to generate a reactive species that inactivates the β-lactamase.
66
Q

What is clavulanic acid?

A
  • Clavulanic acid is an irreversible inhibitor of class A β-lactamases (penicillinases).
  • It has weak antibiotic activity on its own, but it potentiates the effect of penicillins
  • Use of co-amoxyclav partly over-comes bacterial resistance to penicillins.
67
Q

What is the herpes virus?

A

Structure
- Spherical iscoahedron, 150-200 nm
- Double-stranded DNA, linear
- Enveloped

Features
- Establish latent infections
- Lifelong persistence
- Significant cause of death in immunocompromised hosts
- Some can cause cancers

68
Q

What are the three herpesvirus families?

A

Alpha herpesviruses
- Herpes simplex virus type 1 (HSV-1)
- Herpes simplex virus type 2 (HSV-2)
- Varicella-zoster virus (VZV)

Beta herpesviruses
- Cytomegalovirus (CMV)
- Human herpesvirus 6 (HHV-6)
- Human herpesvirus 7 (HHV-7)

Gamma herpesviruses
- Epstein-Barr virus (EBV)
- Human herpesvirus 8 (HHV-8)

69
Q

What is the difference between HSV-1 and HSV-2?

A

HSV-1: oropharyngeal sores (children)
HSV-2: genitalia (young adults)

70
Q

What is Acyclovirand what 3 diseases is it used for?

A

Anti-viral
Inhibition of viral synthesis of DNA
Topical, oral, and intravenous formulations
~20% oral bioavailability

Used for:
- HSV-1/2
- VZV
- possibly EBV

71
Q

What is the MoA of acyclovir?

A

Acyclovir is a pro-drug. It needs to be phosphorylated to acyclovir tri-phosphate to be active.

Acyclovir is a chain terminator. It acts by being incorporated into the replicating viral DNA strand and blocking further replication.

72
Q

What are the 3 first line treatments of HSV-2?

A

Acyclovir 400 mg three times a day for 7-10 days

Valacyclovir (Valtrex) 1000 mg twice a day for 7-10 days

Famciclovir (Famvir) 250 mg three times a day for 7-10 days

73
Q

What is Valacyclovir and its 4 common side effects?

A

L-valyl ester prodrug of acyclovir
Rapidly and almost completely converted to acyclovir
Adverse effects
- Headache
- Nausea
- Dizziness
- Confusion

74
Q

What is Famciclovir?

A

Converted to pencyclovir in the liver and intestines
Available orally only
Used for:
- HSV-1/2
- VZV
- sometimes EBV

Adverse effects:
- Headache
- GI upset

75
Q

What is the Varicella-Zoster Virus?

A

Belongs to the alpha herpesvirus subfamily
Double stranded DNA
Enveloped virus

76
Q

What is the prevalence of VZV?

A

Varicella (chicken pox) is one of the classic diseases of childhood, with the highest prevalence occurring in the 4 - 10 years old age group.
Varicella is highly communicable, with an attack rate of 90% in close contacts.
Most people become infected before adulthood but 10% of young adults remain susceptible.

77
Q

What is the basic pathogenesis of VZV?

A
  • Entry via the respiratory tract
  • Spreads to the lymphoid system
  • Main target organ is the skin (fever and a widespread vesicular rash)
  • Virus remains latent in the cerebral or posterior root ganglia
  • In 10 - 20% of individuals, a single recurrent infection occurs after several decades (shingles).
78
Q

What is Herpes Zoster?

A

Shingles
Herpes Zoster mainly affect a single dermatome of the skin.
It may occur at any age but the vast majority of patients are more than 50 years of age.

Herpes zoster affecting the eye and face may pose great problems.

79
Q

How is Varicella managed?

A

Uncomplicated varicella is a self limited disease and requires no specific treatment.
Acyclovir should be given promptly to immunocompromised individuals with varicella infection and normal individuals with serious complications such as pneumonia and encephalitis.

80
Q

How is Herpes Zoster managed?

A

Herpes zoster in a healthy individual is not normally a cause for concern.
The International Herpes Management Forum recommends that antiviral therapy should be offered routinely to all patients over 50 years of age presenting with herpes zoster.

81
Q

What is the structure of HIV?

A

Icosahedral (20 sided), enveloped retrovirus.
Retroviruses transcribe RNA to DNA.
ssRNA virus
Contains:
- 2 copies of RNA

Enzymes:
- Reverse Transcriptase
- Integrase
- Protease

82
Q

What are fusion inhibitors?

A

It works by blocking the entry of HIV into cells (CD4 or T cells)

83
Q

What is the mechanism of Fuzeon?

A

Fuzeon is a peptide mimic of the HR2 region of gp41.
As a result, Fuzeon binds to the HR1 region.
Zipping cannot take place, and so infection is blocked.

84
Q

What are CCR5 inhibitors?

A

Maraviroc blocks the attachment of HIV to the CCR5 receptor, halting HIV replication.
CCR5 inhibitors like Maraviroc are only effective in blocking that site.
However, the HIV that uses CXCR4 receptors will be unaffected, meaning replication can continue.

85
Q

What are integrase inhibitors?

A

During reverse transcription, the virus has to integrate its genetic material into the genetic material of host cells, this is done by integrase.
Integrase inhibitors block this enzyme and prevent the virus from adding its DNA into the DNA in CD4 cells.

86
Q

What are nucleoside RV inhibitors?

A

Reverse transcriptase inhibitors act as chain terminators or inhibitors at the substrate binding site of RT

87
Q

What are non-nucleoside RV inhibitors?

A

A diverse group of compounds that induce allosteric changes in reverse transcriptase, rendering it incapable of converting viral RNA to DNA. They are structurally diverse.

88
Q

What are protease inhibitors?

A

During the reproduction cycle of HIV a specific protease is needed to process polyproteins into mature HIV components.

All approved PI’s contain a hydroxyethylene bond instead of a normal peptide bond which are non-scissile.

89
Q

What is HAART?

A

Highly active anti-retroviral therapy
There are currently six different “classes” of HIV drugs. Each class of drug attacks the virus at different points in its replication cycle

HAART generally take 3 differentanti-retroviraldrugs from at least 2 different classes. Reduces incidence of resistance.

90
Q

What are the 5 types of vaccine?

A
  • Live–attenuated vaccines (Eg. Measles, Mumps, Rubella)
  • Inactivated (Eg. Hepatitis A, Influenza, Pneumococcal polysaccharide)
  • Recombinant sub-unit (Eg. Hepatitis B)
  • Toxoid (Eg. Tetanus, Diphtheria)
  • Conjugate polysaccharide-protein (Eg. Pneumococcal, meningococcal, Haemophilus influenzea type b (Hib) )
91
Q

What are live-attenuated viruses?

A

Live vaccines are derived from disease-causing viruses or bacteria. They are attenuated in a laboratory usually by repeated culturing.

In order to produce an immune response, live attenuated vaccines must replicate in the vaccinated person. A relatively small dose of virus or bacteria is given, which replicates in the body and creates enough virus to stimulate an immune response.

Pros:
- cheap
- adjuvants

cons:
- potential to cause pathogenicity
- stabilty

92
Q

What are inactivated vaccines?

A
  • cultured pathogen then killed
  • cannot cause disease
  • Needs two or three doses

Pros:
- Generally safer
- Improved stability

Cons:
- Can be costly
- Hypersensitivity

93
Q

What are recombinant sub-unit vaccines?

A

Sub-unit vaccines are comprised of one antigenic part of the pathogen.

The antigenic components are often proteins, or surface polysaccharides.

The immune response to a pure polysaccharide vaccine is typically T-cell independent, which means that these vaccines are able to stimulate B-cells without the assistance of T-helper cells.

94
Q

What are toxoids?

A

Toxoids are forms of chemically altered toxin that are no longer pathogenic.

The antibodies produces in the body as a consequence of toxoid administration neutralize the toxic moiety produced during infection rather than act upon the organism itself. In general toxoids are highly efficacious and safe immunizing agents

95
Q

What are conjugate polysaccharide vaccines?

A

Prepared from extracted cellular fractions

As carbohydrates themselves do not illicit a T-cell response, the polysaccharides are often chemically attached to a carrier protein. Carrier proteins can often be toxoids, such as Tetanus toxoid.

Their efficacy and safety appear to be high.
Conjugate polysaccharide vaccines typically target childhood diseases

96
Q

What are 4 reasons why we need adjuvants?

A
  • stronger and longer to enhance immune response
  • antigen-sparing to induce protective antibody responses with less antigen
  • cross-reactive immunity t induce broader immune response
  • to overcome weakened immunity
97
Q

What are the three Cs of vaccine hesitancy?

A
  • complacency
  • convenience
  • confidence

MPharm2 SL22105 (8 decks)

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