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Sem 5 > Pharmacology 5: Antiviral and antimicrobial agents > Flashcards

Pharmacology 5: Antiviral and antimicrobial agents Flashcards

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1
Q

describe the main steps in how a virus gains entry into a cell and undergoes uncoating

A
  • invading virion (outer protein capsid and nucleosome core- DNA/RNA, ss/ds) attaches to neuraminic acid or sialic acid residue on membrane glycoprotein
  • complex allows viral entry by endocytosis
  • ATP driven H+ entry into endosome, lowers pH, allows fusion of viral membrane with endosomal membrane following conformational change in haemagglutinin on virus
  • H+ enter virus itself via M2= viral ion channel in its envelope, and nucelocapsid of virus subsequently breaks down
  • RNA then escapes into host cell cytoplasm
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2
Q

why might widespread use of M2 ion channel blockers for influenza type A be limited?

A

M2 mutations in H5N1 viruses

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3
Q

examples of M2 ion channel blockers?

A

rimantadine, amantadine

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4
Q

ADRs of M2 ion channel blockers?

A 
dizziness
GI disturbances
hypotension
confusion
insomnia
hallucinations- problematic in elderly as amy already be present, further exacerbated.
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5
Q

how do oseltamivir and zanamivir target influenza?

A

block virion release from host cell membrane by binding to neuraminidase which is required to break the bond between the newly formed virus and the sialic acid residues on the PM to allow virion release

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6
Q

why can oseltamivir be given orally for both tment and prophylaxis?

A

prodrug which is well absorbed, with 80 % bioavailability- so most of the drug reaches the systemic circulation in an unchanged form where it can then exert its desired therapeutic effect..
BUT zanamivir= given as aerosol, low bioavailability, can only be used for tment.

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7
Q

ADRs of neuraminidase inhibitors?

A

GI disturbances
headache
nose bleed (epistaxis)
rarely resp depression, bronchospasm.

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8
Q

viral group to which influenza belongs?

A

orthomyxovirus in the family of RNA enveloped viruses

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9
Q

indication other than influenza for amantadine?

A

Parkinson’s disease: bradykinesia
rigidity
resting tremor

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10
Q

antibiotics which affect DNA synthesis?

A

quinolones e.g. ciprofloxacin- can be used in pyelonephritis, RTIs- but not pneumococcal pneumonia
folic acid antagonsits e.g. trimethoprim- used in UTIs, sulphonamides- CYP 450 inhibitors, e.g. sulfamethoxazole

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11
Q

antibiotics which inhibit protein synthesis?

A

aminoglycosides e.g. gentamicin
macrolides e..g. erythromicin, azithromicin
tetracyclines

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12
Q

antibiotics which inhibit bacterial cell wall synthesis?

A

beta-lactams e.g. penicillins, cephalosporins e.g. ceftriaxone and carbapenems
glycopeptides e.g. vancomycin- S.aureus

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13
Q

give an overview of the general process involved in viral replication

A
  • virus ATTACHES to host cell membrane via proteins on viral surface which bind specifically to host cell membrane components.
  • ENTRY e.g. endocytosis
  • entry into endosome where UNCOATING takes place with loss of capsid proteins following H+ entry, so viral membrane can fuse with endosomal membrane to allow nucleic acid release into host cell cytoplasm.
  • REPLICATION of genome to produce new RNA
  • TRANSCRIPTION-RNA polymerase
  • TRANSLATION, to produce viral protein
  • ASSEMBLY- viral proteins assemble with viral genomes within host cell
  • EGRESS- virus leaves host cell**Influenza viruses- virions require additional step of release from EC surface of host cell membrane.
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14
Q

how does viral life cycle different between retroviruses e.g. HIV and most other viruses

A

viral genome actually incorporated into host cell genome

virus has reverse transcriptase enzyme- converts viral RNA into cDNA.

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15
Q

what are haemagglutinin, neuraminic acid and sialic acid??

A

Haemagglutinin- glycoprotien on surface of influenza viruses which allows attachment to host cells in order to enter via RME by binding to cells with sialic acid on their membranes e.g. cells of URTI.
sialic acid= derviative of neuraminic acid, which is found on the plasma membrane of cells.

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16
Q

what limits the use of M2 channel blockers to treat influenza A?

A

rapid development of resistance- channel within virus changes shape so when drug binds, rather than sitting inside the channel and blocking it, it now lies outside of the channel.

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17
Q

why is rimantadine preferred to amantadine?

A

less ADRs e.g. neurological effects that are especially problematic in elderly. Neur effects due to action on host ion channels likely account for ability of amantadine to be used to treat Parkinson’s disease- rigidity, resting tremor, bradykinesia. related to ability of amantadine to cross BB barrier?

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18
Q

describe the differences between the 3 types of Influenza virus

A 
A= most severe, exhibits antigenic shift and drift, bird(avian) flu. SHift exhibited as doesn't just infect humans.
B= only in humans, more antigenic drift.
C= least severe, common cold. Can be antigenic drift.
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19
Q

how do vaccines target influenza virus (flu vaccination)?

A

cause antibody production in host against haemagglutinin on surface on influenza virus, preventing viral attachment to host cells, so unable to enter.

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20
Q

subtype of influenza A virus known as bird flu/avian flu?

A

H5N1
can be transmitted from birds to humans
(swine flu-pigs-H1N1)

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21
Q

describe the differences between antigenic drift and shift

A 
drift= exhibited by both A, B and C influenza viruses. Mutations in genes encoding antibody binding sites on virus accumulate over time in a known strain of influenza.
shift= 2 or more different strains of a virus, or strains of 2 or more different viruses combine to form a new viral subtype with a mixture of antigens on its surface from the 2 strains.
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22
Q

types of hepatitis virus- what group are they in, drug tments?

A

A- RNA non-enveloped- faecal-oral transmission
B- DNA enveloped- direct contact- blood or body fluids
C- RNA non-enveloped- direct contact- blood, no vaccine available.

B= tenofovir

signs and symptoms hep a and b= abdom pain, jaundice, fever, vomiting, nausea, diarrhoea.
all causes of liver cirrhosis.

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23
Q

people at high risk of complications from influenza virus?

A 
COPD patients
asthma patients
renal failure patients
diabetes patients
CVD patients
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24
Q

complications of influenza virus?

A

bronchitis
pneumonia
sinusitis
exacerbation of underlying disease

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25
symptoms of influenza?
``` sudden high temperature headache general aches and pains tiredness nausea appetite loss sore throat ```
26
how can influenza be transmitted?
inhalation- droplets direct contact indirect contact
27
what type of influenza are M2 ion channel blockers active against?
only influenza A
28
example of mutation conferring resistance of influenza A virus to M2 ion channel inhibitors?
S31N= single point mutation | responsible for resistant H5N1 isolates (avian flu)
29
why can neuraminidase inhibitors be used against more subtypes than just influenza A?
active site of enzyme is conserved across virus subtypes
30
overall mechanism of action of neuraminidsase inhibitors?
block viral release from host cell by binding to active site of enzyme responsible for allowing separation of haemagglutinin protein on virus surface from sialic acid residue on host cell to enable virus to be released. enzyme cleaves sialic acid from membrane glycoproteins.
31
what is zanamivir?
a sialic acid analogue capacle of binding to the neuraminidase enzyme to inhibit it from allowing influenza viral release from host cell. active against influenza A and B but poor oral bioavailability as would be destoryed in stomach, so must be administered by inhaler (aerosol).
32
how has it been shown that oseltamivir reduces mortality?
Canadian study showed drug could offer approx. 70% mortality reduction. This was achieved even when dosing as delayed as 64hrs after symptom onset.
33
difference in structure of bacteria which are gram +ve and gram -ve?
gram +ve= cell wall is 2 layers- 1 being thick peptidoglycan layer which doesn't allow extraction of complex extraction in gram staining so is stained purple. gram -ve= 3 layered cell wall, peptidoglycan layer thin so allows complex extraction, so now unstained in gram staining and red dye allows added which stains the bacteria, so appear red.
34
describe how O2 therapy is given to a COPD patient in the acute setting?
aiming for O2 saturation of 88-92%, in contrast to 94-98% in patients without COPD. O2 given at no more than 28% via venturi mask- high flow O2 therapy, known conc of O2 given, prevents CO2 retention. ABGs must be checked within 1 hr of starting supplemental O2 or changing its conc.
35
antibiotics used to treat pneumonia in a penicillin allergic patient?
so can't use amoxicillin or co-amoxiclav, latter used in more severe cases- as determined by CURB-65 score: age 65 or more, confusion-GCS, urea >7mmmol/l, resp rate>/= to 30 breaths per min, BP <60mmHg diastolic. can give macrolide e.g. erythromycin, or tetracycline e.g. doxycycline.
36
TB drugs and how long?
rifampicin- 6 months isoniazid- 6 months pyrazinamide- first 2 months ethambutol- first 2 months
37
tests to be done before starting TB drug therapy?
liver function tests- as rifampicin, isoniazid and pyrazinamide assoc with liver toxicity renal function tests- Us and Es, ethambutol should be pref avoided in patients with renal impairment FBC test for visual acuity-Snellen chart, as ethambutol can cause visual acuity loss, colour blindness and restriction in visual fields. HIV baseline test
38
tment for patient if screen +ve for TB but is asymptomatic?
6 months isoniazid
39
drug tment for bacterial endocarditis caused by streptococcus viridans?
benzylpenicillin- common ADR=hypersensitivity reactions in allergic patients. gentamicin given for 4-6 wks, gentamicin stopped after 2 vancomycin if penicllin allergic
40
monitoring of patients required if taking gentamicin?
Renal function should be assessed before starting an aminoglycoside and during treatment. Auditory and vestibular function should also be monitored during treatment. In order to optimise the dose and avoid toxicity, serum-aminoglycoside concentrations should be monitored in patients receiving parenteral aminoglycosides. Ototoxicity and nephrotoxicity occur most commonly in the elderly; therefore, monitoring is particularly important in these patients, who may require reduced doses.
41
drug other than gentamicin that can cause ototoxicity?
furosemide= loop diuretic
42
enzyme which quinolones targeting DNA synthesis in bacteria interfere with?
DNA gyrase
43
type of ribosomal RNA interfered with by antibiotics targeting protein synthesis?
16S ribosomal RNA (part of 30S ribosomal subunit)= tetracyclines 23S rRNA= bound to by those targeting 50S ribosomal subunit e.g. macrolides and chloramphenicol * contrast to 18S ribosomal RNA found in eucaryotes as part of 40S ribosomal subunit
44
macrolide used in H pylori eradication?
clarithromycin
45
why is selective toxicity of beta-lactams and glycopeptides more so than that of other antibiotics?
targeting cell wall synthesis, only present in bacteria, not in eukaryotes
46
antibiotics classed as beta-lactams?
penicillins cephalosporins carbapenems
47
how is resistance to macrolides usually manifested?
it is plasmid-encoded, and may involve the production of esterases that hydrolyse macrolides. ribosomal binding site may also be modified.
48
how do aminoglycosides work?
interfere with protein synthesis by binding to 16S rRNA of 30S subunit (tetracyclines also do this)
49
hoe does rifampicin, used in TB tment, work?
inhibits bacterial RNA polymerase, so inhibits transcription
50
how do quinolones e.g. ciprofloxacin act?
inhibit DNA gyrase and topoisomerase IV
51
how do glycopeptides interfere with cell wall synthesis?
inhibit peptidoglycan polymerisation
52
how is antibiotic activity measured?
disc sensitivity testing= antibiotic disc placed on agar plates of of bacteria. antibiotic diffuses in agar, further away from disc= lower conc of antibiotic. Larger zone around disc absent of bacteria= most sensitive to that antibiotic. > than a set diameter= sensitive.
53
who is given prophylaxis for bacterial infections?
peri-operative= prevent surgical site infections e.g. use of metronidazole or amoxicillin before gut surgery ST= meningitis contacts LT= asplenia= also given vaccination against encapsulated bacteria= N.meningitidis, H.influenzae and S.pneumoniae, AND medical alert bracelet immunodeficiency
54
why might antibiotic thought to work from susceptibility data not work in a patient?
organism tested on agar plate isn't causing the infection dose of antibiotic is inappropriate antibiotic isn't getting to site of infection
55
what is the minimum inhibitory concentration?
Minimum concentration of antibiotic required to inhibit growth of a bacterium in vitro Units are mg/l (or equivalently μg/ml) Antibiotic and isolate specific higher value= bacterium is less sensitive to that antibiotic. =E tests, may be used e.g. for vancomycin as on disc testing, diameter for bacteria which are sensitive and not sensitive isn't much different.
56
gentamicin is effective against N.meningitidis in vitro, why can it then not be used to treat meningitis?
unable to cross BB barrier
57
main routes of antibiotic administration?
oral | IV
58
why are antibiotics not given intrathecally e.g. for meningitis?
can cause seizures and encephalopathy as reach concns toxic to CNS
59
2 types of pharmacodynamic classes of antibiotics?
concentration dependent killing | time dependent killing
60
characteristics of antibiotics which work by time dependent killing?
Successful treatment requires prolonged antibiotic presence at site of infection don't need a high concentration, just a concentration which is higher than the MIC= minimum conc of drug required to inhibit growth of bacterium in vitro. e.g. penicillins, cephalosporins e.g. ceftriaxone, and glycopeptides e.g. vancomycin= cell-wall dependent so need to give frequent doses to ensure antibiotic always present at site of infection e.g. continuous infusion.
61
what is concentration dependent killing?
type of pharmacodynamic class of antibiotics antibiotic needs high Cmax/MIC ratio Successful treatment requires high antibiotic concentration at site of infection= achieved by giving a high dose- only need high dose once daily= this reduces risk of ADRs. But don't want antibiotic there for long e.g. aminoglycosides e.g. gentamicin, and quinolones
62
genetic mechanisms underlying antimicrobial resistance?
chromosomal mutation | horizontal gene transfer
63
ADRs of penicillins?
hypersensitivity reactions encephalopathy electrolyte disturbances diarrhoea, C-difficile infection
64
ADRs of cephalosporins?
C difficile infection, diarrhoea hypersensitivity reactions disturbances in liver enzymes nausea, vomiting, abdom discomfort
65
ADRs of carbapanems?
hypersensitivity neurotoxicity C difficile infection
66
ADRs of tetracyclines?
renal and liver toxicity C difficile infection nausea and vomiting and diarrhoea
67
ADRs of macrolides?
nausea, vomiting, diarrhoea
68
ADRs of chloramphenicol- inhibits bacterial 50S ribosomal sub-unit?
adverse effect on BM- suppressed
69
ADRs of glycopeptides?
hypersensitivity renal toxicity ototoxicity effect on BM
70
antibiotics requring therapeutic drug monitoring?
aminoglycosides | vancomycin= glycopeptide
71
what markers can be monitored to assess for toxicity with antibiotics?
``` creatine kinase- daptomycin eosinophils- daptomycin FBC- chloramphenicol renal function -aminoglycosides auditory function- aminoglycosides stool chart- most antibacterials in hospital to check for C difficile infection. ```
72
which antibiotics may interact with anticoagulants, increasing risk of bleeding?
penicillins cephalosporins tettracyclines chloramphenicol

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