Question book 5 Flashcards
21 year old from Colombia, 21 weeks pregnant
Presents with morbilliform rash, conjunctivitis, fever
develops pneumonitis
Which therapy is advocated for this patient?
ribavirin aciclovir paliziumab measles specific IgG human normal immunoglobulin
human normal immunoglobulin
suggestive of measles - and may be unvaccinated
HNIG can attenuate disease if given early to immunocompromised, pregnant, or infants <9 months (who will be unvaccinated)
26 year old, 16 weeks pregnant, has fever nad URTI
Influenza A confirmed
Started on oseltamivir
What is mechanism of action of oseltamivir?
inhibits neuraminidase cleavage of budding virions
inhibits haemagglutinin binding to epithelial sialic acid
inhibits dissociation of viral ribonuclearproteins
inhibits neuraminidase preventing virion epithelial entry
inhibits epithelial endosome fusion with the viral membrane
inhibits neuraminidase cleavage of budding virions
influenza binds to sialic acid on host epithelial cells through haemagluttinin, and then gains access through endosome fusion.
Neuraminidase normally cleaves sialic acid, to allow new virions to bud from cell
which of the following is not used for treatment against the specified virus
lamividuine HIV lamivudine and HBV amantadine and influenza B ribavirin and RSV aciclovir and HSV
amantadine and influenza B
amantadine inhibits with M2 ion channel in influenza A, preventing uncoating.
influenza B has different structure of M2, so oseltamivir is ineffective
lamivudine inhibits reverse transcriptase - HBV/ HIV
aciclovir inhibits thymidine kinase thereby inhibiting DNA polymerase of herpes viruses
What is mechanism of action of fusidic acid
binding to ribosomes and dissociation of peptide-tRNA
inhibition of topoisomerase IV
inhibition of protein synthesis at 30S subunit
interference with pencillin binding protein activity
binding with elongation factor G and interference with protein synthesis
binding with elongation factor G and interference with protein synthesis
fusidic acid only effective on gram pos bacteria
fusidic acid is bacteriostatic
Discharging wound grows Staph aureus
Antibiogram shows resistance to penicillin, fusidic acid and gentamicin
What is the main mechanism whereby staphylococcal gains resistance to aminoglycoside therapy
ribosomal binding site alteration
aminoglycoside degrading enzyme production
loss of porin channels
up-escalation of efflux mechanisms
alteration of cell wall d-ala-d-ala cross linkage
aminoglycoside degrading enzyme production
3 types of aminoglycoside resistance:
- reduced uptake/ reduced cell permeability - common in Pseudomonas and other gram negatives
- alterations to ribosomal binding site - uncommon as ribosome has multiple binding sites, so needs multiple mutations
- production of aminoglycoside modifying enzymes (most common) - enzymes usually found on plasmids or transposons
What is mechanism of aminoglycoside post-dose effect
prevention of cross-linking of peptide chains
inhibition of cell wall synthesis
binding to protein G and inhibition of protein synthesis
inhibition of ribosomal function
inhibition of topoisomerase IV
inhibition of ribosomal function
aminoglycosides damage cell membrane, and bind to 30S subunit of ribsome
need once a day dosing, as there post-dose effect is to block ribosomes from functioning
Plan to use amoxicillin in pregnant patient who has LRTI/
Which pregnancy safety category is amoxicillin classed under
Category A Category B Category C Category D Category X
Category B
FDA guidelines
Cat A - randomised controlled trial shows it is safe
No RCT in pregnant women, but penicillin known to be safe
Patient with CNS TB
Which drug is best for crossing BBB
rifampicin isoniazid ethambutol streptomycin pyrazinamide
isoniazid
34 year old with drug-susceptible TB, commenced on quadruple therapy.
Remains smear positive at 2 months
Therapeutic drug monitoring showed low levels of some of anti-mycobacterials
Genetic testing showed that he was a fast acetylator
Which drug is affected by this genetic mechanism
isoniazid rifampicin pyrazinamide ethambutol moxifloxacin
isoniazid
N-acetyletransferase is an enzyme involved in isoniazid clearance, and genetic variation (fast acetylators) can lead to fast clearance of isoniazid
What is mechanism whereby Streptococcus pneumoniae can display phenotypic resistance to both erythromycin and clindamicin
efflux pump enzymatic degradation porin loss target alteration impermeability
target alteration
macrolide erythromycin and lincosamides clindamicin insert into 23S subunit of 50S ribosome - blocking protein assembly
This is bactericidal for S.pneumoniae
mutation in ermB gene encodes resistance to both drugs - and alters target site at ribosome
At which site do the fluoroquinolone class of antimicrobials act
cell wall synthesis DNA-dependent RNA polymerase RNA-dependent DNA polymerase Topoisomerase IV ribosomal protein synthesis
Topoisomerase IV
Quinolones act on:
DNA gyrase of gram negative bacteria
topoisomerase for gram pos bacteria
What is the mechanism of action of rifampicin
cell wall inhibitor DNA gyrase inhibitor DNA-dependent RNA polymerase inhibitor DNA-dependent DNA polymerase inhibitor Folate inhibition
DNA-dependent RNA polymerase inhibitor
resistance caused by alteration of rpoB gene which encodes part of ribosome subunit
What is main side effect of rifampicin therapy
eighth nerve toxicity optic neuritis hepatitis dental discolouration pulmonary fibrosis
hepatitis
optic neuropathy caused by ethambutol or linezolid
peripheral neuropathy caused by isoniazid or linezolid
eighth nerve toxicity caused by aminoglycosides
dental discolouration caused by tetracyclines
pulmonary fibrosis caused by nitrofurantoin
23 year old with enteritis and Campylobacter jejuni detected in stools by PCR
what is suitable antimicrobial therapy
amoxicillin ciprofloxacin tetracycline azithromycin ceftriaxone
azithromycin
most cases do not require antibiotics
if severe infection - e.g fever/ hypotension or immunosuppressed, then may require treatment
22% rate of fluoroquinolone resistance UK. Even higher if campylobacter imported by traveller
C. jejuni causes 90% UK infections
C. coli causes other 10%
65 year old diagnosed with paucibacilliary leprosy
What is an essential component of the treatment regime?
isoniazid moxifloxacin dapsone clarithromycin clofazimine
dapsone
Paucibacilliary - ( lepromatous) one or more hypopigmented macules
Treatment is dapsone + rifampicin for 6 months
Multibacilliary (tuberculoid) - symmetrical skin nodules with thickened dermis
Treatment is dapsone + rifampicin + clofazimine for 24 months
65 year old with paucibacilliary leprosy - commenced on dapsone and rifampicin. Develops rash and eosinophilia
What is most likely diagnosis
agranulocytosis allergic dermatitis stevens-johnson syndrome toxic epidermal necrolysis dapsone syndrome
dapsone syndrome
On spectrum of DRESS (Drug relation eosinophilia with systemic symptoms)
presents with rash, fever, eosinophilia
