PHARM: Antibiotics + Antivirals Flashcards
(41 cards)
1
Q
directed vs empirical vs prophylactic Tx
A
- directed: when we know what the pathogen is
- empirical: when we don’t know what the pathogen is - ‘best guess’/broad spectrum
- prophylactic: preventative when there is a significant risk of infection
2
Q
4 features of an ideal therapeutic agent
A
- gets to site of infection
- destroys pathogen but not host (selective toxicity)
- stays @ target site long enough to be effective
- eliminated from body w/o causing harm
3
Q
why do we target folate synthesis as a target in bacteria? which antibiotic does this?
A
- b/c humans can get folate from diet whereas bacteria can only synthesise it endogenously
- trimethoprim, methotrexate
4
Q
why is protein synthesis a good target in bacteria?
A
- difference in bacteria vs animal cell ribosomes
5
Q
when would we use bacteriostatic vs bactericidal antibiotic?
A
- bacteriostatic: healthy immune function
- bactericidal: immunocompromised ppl h/w need to consider that dying gram -ve bacteria can release endotoxins, gram +ve bacteria release exotoxins
6
Q
MIC vs MBC vs MEC
A
- MIC: minimum inhibitory concentration (bacteriostatic)
- MBC: minimum bactericidal concentration
- MEC: minimum effective plasma concentration
7
Q
time-dependent antibiotics + examples
A
- increasing dose does not increase effect, just need to maintain effect for a certain period of time
- e.g. B-lactams (penicillins + cephalosporins)
8
Q
concentration-dependent antibiotics + examples
A
- increasing dose increases effect
- e.g. aminoglycosides,
fluoroquinolones
9
Q
superinfection
A
- new infection occurring in a Pt that is being treated for an existing condition
- due to imbalance of microflora
- e.g. C. difficile infection after antibiotics
10
Q
MIND ME antimicrobial creed
A
- Microbiology-guided therapy (knowing the pathogen first)
- Indications are evidence based
- Narrowest spectrum possible
- Dosage personalised to Pt
- Minimise duration of therapy
- Ensure oral therapy when appropriate
11
Q
why is it difficult to get broad spectrum antivirals?
A
- they differ so much in their structure so can’t get one that targets many viruses
12
Q
do virucidal drugs exist?
A
- no, only virustatic
- viruses are not living so can’t kill them
13
Q
why do viruses become resistant to drugs?
A
- mutate very quickly
14
Q
should we always take antivirals?
A
- no, this can lead to resistance as not necessary
- immune system = best defence
15
Q
high risk populations for viruses
A
- pregnant women
- newborns
- elderly
- immunocompromised
16
Q
which viruses have antiviral Tx?
A
- herpesviridiae: herpes simplex virus, varicella-zoster virus, cytomegalovirus
- influenza
- hep B and C
- RSV (respiratory syncytial virus)
- HIV
17
Q
examples of antiretroviral (ART) drug classes
A
- reverse transcriptase inhibitors (nucleoside or non-nucleoside) - NRTI or NNRTI
- protease inhibitors
- entry inhibitors
- integrase inhibitors
18
Q
adverse effects to antivirals
A
- headache, malaise (general discomfort), fatigue e.g. guanine analogs and neuraminidase inhibitors
- dose-limiting toxicity e.g. hepatomegaly
- significant drug interactions e.g. protease inhibitors for HIV
19
Q
aim of ART (antiretroviral) - HIV Tx
A
- achieve maximal and durable suppression of viral load
- restore or preserve immune function
- resolve symptoms of HIV infections
> improve QOL - reduce mortality
- prevent HIV transmission
20
Q
best type of Tx for ART
A
- combination therapy
- 3 or more drugs from 2 or more classes
- fixed dose combinations available (in one tablet) to increase Pt compliance
- e.g. HAART (highly active antiretroviral therapy)
21
Q
when is the CD4 count considered AIDS and how many do we want ideally?
A
- CD4 count < 200
- ideally we want 500+
22
Q
penicillin: class, MOA, adverse effects, example, how is it excreted?
A
- B-lactams (bactericidal - gram +ve)
- MOA: irreversibly inhibits transpeptidases which facilitate cross-linking and strengthening of the cell wall
- adverse effects: allergies, superinfection
- e.g. amoxicillin (generally 1st line Tx)
- excreted renally
23
Q
cephalosporins: class, MOA, contraindication, side effects, example
A
- B-lactams (bactericidal against gram +ve and -ve)
- MOA: irreversibly inhibits transpeptidases which facilitate cross-linking and strengthening of the cell wall
- can be contraindicated in Pts w/ penicillin allergy
- GI issues (‘lex’ sounds like laxative)
- e.g. cephalexin
24
Q
glycopeptides: MOA, adverse effects, examples
A
- bactericidal (gram +ve only)
- MOA: irreversibly inhibits transglycosidase enzyme > inhibits cell wall synthesis
- adverse effects: red man syndrome (vasodilation from rapid IV administration), ototoxicity, nephrotoxicity
- e.g. vancomycin (ambulance Van = Red Cross = gram +ve, also Red man’s) - used for MRSA or B-lactam allergies
25
trimethoprim: MOA, adverse effects
- MOA: inhibits folate USE by inhibiting DHF (dihydrofolate) reductase
- adverse effects: allergies
26
sulphonamide MOA
- inhibits folate synthesis
27
macrolides: MOA, adverse effects, example, what is it used for
- bacteriostatic
- MOA: reversibly binds to 50s ribosomal subunit + interferes w/ bacterial protein synthesis
- adverse effects: cardiotoxic (arrhythmias), hepatotoxic, GIT issues
- e.g. erythromycin (THR = THREE trimesters = contraindicated in pregnant Pts)
- 2nd line Tx for Pts allergic to penicillin
- used for URTIs
28
chloramphenicol: class, MOA, adverse effects
- class: chloramphenicol (bacteriostatic)
- MOA: reversibly binds to 50s ribosomal subunit, preventing peptide bond formation
- adverse effects: grey baby syndrome, abdominal distention, grey discolouration
- "chlor" = chlorine = drowning baby = grey baby
29
tetracycline: MOA, adverse effects, contraindications, example
- bacteriostatic
- MOA: reversibly binds to 30s ribosomal subunit, preventing protein synthesis
- adverse effects: chelates (depletes) Ca2+, teeth discolouration, decreased bone growth in children under 8, photosensitivity, nephrotoxic, hepatotoxic
- contraindications: children younger than 8 and pregnant women after 18 weeks
- e.g. doxycycline
30
aminoglycosides: MOA, adverse effects, examples
- bactericidal (broad spectrum, gram -ve aerobes)
- MOA: irreversibly binds to 30s ribosomal subunit > misreads mRNA
- adverse effects: nephrotoxicity, ototoxicity
- gentamicin, streptomycin
31
fluoroquinolones: MOA, adverse effects, examples
- bactericidal
- MOA: inhibits DNA replication by inhibiting topoisomerase
- adverse effects: cartilage and tendon damage, phototoxicity
- e.g. ciprofloxacin
32
nitroimidazole: MOA, adverse effects, example
- bactericidal (anaerobes - metro = train = train can't breathe)
- MOA: inhibits DNA replication by unwinding DNA (can also target Giardia) - METRO = train tracks = unwind DNA
- adverse effects: metallic taste (metal train tracks), interferes with alcohol metabolism, peripheral neuropathy
- e.g. metronidazole
33
TB treatment
- RIPE
- rifampicin - inhibits RNA polymerase, turns secretions orange and yellow
- isoniazid (1st line) - targets mycolic acid synthesis
- pyrazinamide - mycolic acid
- ethambutol - mycolic acid
34
ritonavir MOA, adverse effects, indication
- MOA: protease inhibitor (pharmacoenhancer - boosts other protease inhibitors by slowing metabolism)
- adverse effects: GI effects, nephrotoxicity, cardiotoxicity
- indication: part of HAART (highly active antiretroviral therapy - HIV)
35
tenofovir: MOA, adverse effects, indication
- MOA: inhibits viral DNA polymerase
- adverse effects: GIT issues
- indication: HIV prophylaxis, chronic hep B
36
aciclovir: MOA, adverse effects, indication
- MOA: DNA polymerase inhibitor
- adverse effects: GIT issues
- indication: herpes simplex, varicella zoster
37
oseltamivir: MOA, adverse effects, indication
- MOA: neuraminidase inhibitor, preventing influenza release from cell
- adverse effects: GIT issues
- indication: influenza A and B Tx and prophylaxis IN IMMUNOCOMPROMISED PTS
38
interferon alpha: MOA, adverse effects, indication
- MOA: stimulate immune response, interferes w/ viral DNA
- adverse effects: headache, fever, chills, myalgia, retinopathy - dose-dependent
- indication: hep B, C and cancer
39
if a bacteria has endotoxins within its cell wall, is it better to use a bacteriostatic or bactericidal antibiotic?
- bacteriostatic
- if given bactericidal, endotoxins (gram -ve) or exotoxins (gram +ve) may be released and cause more harm than good
40
some bacteria have B-lactamase enzymes that break down penicillin drugs - why must penicillin be administered with C-lavulonic acid?
- because C.A. is a suicide component that undergoes breakdown to protect the drug
41
NRTIs vs NNRTIs
- NRTIs: terminate DNA elongation, causing non-viable virions to form.
- NNRTIs inhibit RT enzyme active site > prevent reverse transcription happening
