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FRACP Exam > ID > Flashcards

ID Flashcards

1
Q

What mosquito spreads malaria

A

Anopheles - night time biter

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2
Q

What do positive thick and thin films show?

A

Rings of parasites within RBC

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3
Q

What does the malaria rapid antigen test detect?

A

HRP2
Detects 95% low parasitemia

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4
Q

What are indications for IV arterunate in malaria?

A

Can’t take tabs
End organ disease
Severe disease

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5
Q

What malaria species can be dormant in the liver for years?

A

P.vivax, P ovale

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6
Q

How do you treat relapsing malaria (p.vivax)

A

Primaquine
Tafenoquine

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7
Q

What needs to be checked before starting primaquine?

A

G6PD deficiency

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8
Q

What blood cultures are found with malaria?

A

Gram negative bacteraemia

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9
Q

Onset of illness and fevers in returned traveller <10 days?

A

Dengue
Influ
Zika
Chikungunya
Enteric
Rickettsia
Yellow fever

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10
Q

What illness in returned traveller happen 10-21 days

A

Malaria
VHF
Typhoid
Brucellosis
Leptospirosis

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11
Q

What illnesses occur >21 days in returned traveller?

A

Malaria
Hepatitis
TB

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12
Q

Returned from subsaharah Africa ass with what infection?

A

Malaria

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13
Q

Returned from East Asia + Latin America?

A

Dengue

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14
Q

Returned south central Asia?

A

Enteric fever

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15
Q

What is NS1 antigen panel for?

A

Dengue fever

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16
Q

What are the love vaccines?

A

MMR
Yellow fever
BCG
Varicella/zoster
Oral polio
IMOJEV
Orocol Berna
Oral typhoid

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17
Q

What is long duration of high fevers and relative Bradycardia a feature of?

A

Typhoid

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18
Q

Multi drug resistant typhoid is resistant to what?

A

Amoxi, quinoline, trimethoprim
Sens ceftri, azithro

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19
Q

How.do you treat typhoid from Pakistan?

A

Carbapenem (as resistant++)

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20
Q

What is NS1?

A

Viral protein (Dengue) that disrupts the endothelial gycoxalyx increasing vascular permeability leading to shock

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21
Q

For Dengue what test are done <5 days of infection, and what >5 days of infection

A

< 5 - PCR/NS1
>5 Serology/IgM

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22
Q

Do platelet infusion help with dengue thrombocytopenia?

A

No

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23
Q

What are the guidelines for unprotected sex after travel to Zika endemic country?

A

Men - condom for 3 months (NZ guidelines say 6)
Women - condom 2 months

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24
Q

Chikungunya is associated with what symptom?

A

Arthritis/arthralgia - some develop chronic inflammatory synovitis following infection

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25
Q

How do you treat strongyloides?

A

Ivermectin

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26
Q

What are side effects of rifampicin?

A

Hepatotoxicity, nausea, abdominal pain.
CYP3A4 Inducer, P-gly-p inducer

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27
Q

What are side effects of isoniazid?

A

Hepatotoxicity, peripheral neuropathy (treated by pyridoxine), inhibits cyp450 enzymes

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28
Q

What are the 4 drugs for TB?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

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29
Q

What are side effects of ethambutol?

A

Optic neuropathy - get eyes tested before starting

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30
Q

What is multi drug resistant TB?

A

Resistant to rifampicin AND isoniazid

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31
Q

What gene gives TB resistance to rifampicin?

A

ROPV (don’t usually have isolated rifampicin resistance, usually indicates Isoniazid resistance)

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32
Q

What are the treatment regimens for active tb?

A

RIPE - 2 months, followed by isoniazid+ rifampicin for 4 months
Extend to 9 months total I’d cavitatary disease, meningitis or bone/joint disease

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33
Q

When do you give steroids in TB?

A

TB meningitis + TB pericarditis

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34
Q

What is used in MRD TB?

A

Bedaquilline, pretomanid, linezolid, moxifloxacin

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35
Q

What is the MoA of isoniazid?

A

Inhibits the synthesis of mycolic acid through the NADPH-dependent enoyl-acyl carrier protein ACP reductase

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36
Q

What is the mechanism of drug resistance to isoniazid?

A

It requires mycobacterium catalase peroxidase to be activated - mutations in this confer resistance

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37
Q

What cytokines/chemokines are important in the immune response to TB?

A

T-cell mediated
INF-Y, TNF-A, IL12

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38
Q

How long after exposure to TB will the IGRA, TSPOT, TST tests be helpful?

A

8 weeks - need to have been able to mount a t cell response to have a positive test

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39
Q

Pyrazinamide, isoniazid, rifampicin causw hepatotoxicity, when do you stop treatment?

A

When ALT 3 X ULN with symptoms or ALT>5ULN asymptomatic
Restart when ALT near baseline

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40
Q

What defines XDR-TB? (Extensively resistant)

A

R to isoniy, rifampicin and fluoroquinolones and at least 1 injectable treatment (kanamycin, calreomycin, amikacin)

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41
Q

Can you culture PJP?

A

No, need microscopy/ immunofluorescence for visualisation

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42
Q

What is in maviret?

A

Glecaprevir and pibrentasavir

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43
Q

What is the MoA of Glecaprevir?

A

Inhibits HCV serine protease NS3/4A required for viral maturation

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44
Q

What is the MoA of pibrentasavir?

A

Inhibitor of HCV NS5A which is essential for RNA replication and vision assembly

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45
Q

Can you use glecaprevir+ pibrentasavir in pregnancy?

A

No data, Recommend deferring treatment until post-partum, risk of transmission is low.
Shouldn’t be used in BF either

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46
Q

How do you know treatment has cured HCV infection?

A

Negative HCV core antigen assay at 12 weeks

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47
Q

What surface molecule give HIV entry to cells?

A

GP120 attachedk to GP40 on the virus surface

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48
Q

What do GP120/GP40 attach to

A

CD4 and co-receptor CCR5, or CXCR4

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49
Q

What HLA type leads to more effective clearance of HIV virus?

A

HLAB*57.01 - binds HIV core protein that is essential for HIV replication, and therefore mutants are not able to replicate. Associated with slower progression ( same HLA ass with abacavir hypersens)

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50
Q

What is the MoA of Tenofovir?

A

Reverse transcriptase inhibitor

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51
Q

What is the MoA of Emtricitabine?

A

NRTI - Nucleoside reverse transcriptase inhibitor

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52
Q

What drugs are INSTIs? Intergrase inhibitor

A

Dolutegravir, raltegravir, bictegravid, elitegravir

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53
Q

What drugs are NNRTI? Non-nucleoside reverse transcriptase inhibitor

A

Efavirens, rilpivarine, nevirapine

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54
Q

What HIV med can’t be used in renal failure?

A

Tenofovir TDF - avoid eGFR <60, associated with renal tubulopathy
Tenofovir TAF - less nephrotoxic

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55
Q

What are side effects of zidovudine?

A

Lipodystrophy, central obesity, GI side effects

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56
Q

Side effects of tenofovir?

A

Nephrotoxic, reduced bone mineral density, phosphate wasting in urine. Need to monitor urine P{;Cr

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57
Q

What are the side effects of efaverens?

A

Eff you up - CNS side effects in first few weeks, sedation, insomnia, vivid dresms, neuropsych

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58
Q

What is ritonavir?

A

Protease inhibitor, but usually only used to inhibit CYP3A4 to improve function of/boost other ARTs

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59
Q

What are side effects of raltegravir?

A

can cause rhabdo, increase CK

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60
Q

What are side effects of dolutegravir?

A

Headache, depression/anxiety, raises serum creatinine without renal toxicity, vivid dreams, mood disturbance.

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61
Q

What is maraviroc in HIV treatment?

A

CCR5 inhibitor - doesn’t work if the virus uses CXCR4 coreceptor

62
Q

In HIV at what CD4 count should not have liver vaccines?

A

CD4<200

63
Q

When do you start HART treatment in HIV if TB meningitis and cryptococcal meningitis?

A

Must have treatment of infection for ~8 weeks to acoiif IRIS and increased intracranial pressure / brain herniation

64
Q

When do you start OI prophylaxis in HIV?

A

CD4<200 - start PJP prophylaxis
No live vaccines after CD4<200
CD4<100 - start toxoplasmosis prophylaxis
Can stop Primary prophylaxis when CD4 recovers to 300-400

65
Q

How does cryptococcal meningitis present?

A

Subacute meningitis, increased intracranial pressure/HTN, Cranial nerve palsiea, seizures, confusion, fevers.
CD4 usually < 100
LP: lymphocytix wih low glucose and high protein - Cryptococcal antigen present

66
Q

How do you treat cryptococcus meningitis?

A

Induce with amphoterecin + flucytesine - min 2 weeks then PO fluconazole 8 weeks then maintenance fluconazole.
DELAY ART until treatment commenced in new dx

67
Q

What is the timeframe for PEP?

A

<72 hours - 3 drug if risk >1/1000 for 28 days if unkown or detectable viral load

68
Q

When should live vaccines be avoided in the immunocompromised host?

A

Not while on high dose immunosuppression incl Anti-TNF, and ritux, contraindicated 4 weeks prior to.
Should try vaccinate early as possible prior to immunosuppression.

69
Q

What organ transplant is highest risk of toxoplasmosis ?

A

Cardiac transplant - should have life long prophylaxis

70
Q

What is the MoA of remdesivir and molnupiravir?

A

RdRP (RNA dependent RNA polymerase) inhibitors - preventing viral RNA synthesis

71
Q

What is the MoA of Nortemavir/ritonavir?

A

Protease inhibitors - preventing primary translation and polyprotein processing

72
Q

What receptor does COVID bind to to gain entry into the cell?

A

ACE2 and TMPRSS2

73
Q

What are contraindications to molnupiravir?

A

Pregnant/breast feeding, dialysis, ESRF, ES liver failure

74
Q

What are contraindicatinos to use of remdesivir?

A

eGFR <30, liver disease (ALT >5 x ULN)
SAFE in pregnancy

75
Q

What are side effects of remdesivir?

A

Liver and renal failure

76
Q

What is in evusheld?

A

Tixagevumab, cilgavemab - anti-spike protein MABS

77
Q

What is the half life of evusheld?

A

2-3 months ( ~85 days)

78
Q

Can you use dexamethasone in COVID if NOT hypoxic?

A

No, associated with INCREASED mortality

79
Q

What gene gives MRSA resistance?

A

mecA - encodes the penicillin binging protein 2A, alterations reduce the affinity of betalactam drug binding (resistance to penicillin, cephalosporin and carbapenems)

80
Q

What does M-MRSA mean?

A

Resistant to b-lactam AND 2 or more non-beta lactam antibiotics - eg erythro + clinda, cotrim, gent, rifampicin, fuscidic, mupirocin, tetracyclin, chloramphenicol
OR to cipro

81
Q

What is Panton valentine leucocidin?

A

PVL is a pore-forming necrotising exotoxin that causes leucocyte destruction and tissue necrosis. Present in most community MRSA in USA

82
Q

If MRSA resistant to erythromycin, what will it likely have inducible resistance to?

A

Clindamycin

83
Q

What is the MoA of Linezolid?

A

Binds to 30S and 50S ribosomal subunits inhibiting bacterial proteion synthesis, it is bacteriostatic.
Broad spectrum of action for Gram +

84
Q

What are the side effects of linezolid?

A

Myelosupression (reversible), and peripheral neuropathy

85
Q

What is Daptomycin?

A

Cyclin lipopeptide bactericidal antibiotic that causes depolarisation of the bacterial cell membrane

86
Q

Can you use daptomycin in respiratory tract infections?

A

No - it is inactivated by pulmonary surfactant.

87
Q

What are the side effects of daptomycin?

A

Myopathy, peripheral neuropathy, eosinophilic pneumonia, needs real dose adjustment

88
Q

What is the MoA of Tigecycline?

A

Glycycline antiobiotic, protein synthesis inhibitor - binds 30S ribosomal subunit. Bacteriostatic.
Can use in renal failure as cleared by biliary tract.
Works in MRSA, VRE, ESBL, Amp Cs

89
Q

What is coag negative staph?

A

Staph. epi

90
Q

How is the mechanism of action of Vancomycin?

A

Inhibits synthesis of bacterial cell wall by binding to D-ala-Dala terminuc of the pentapeptide side chain preventing cross linking, actie against Gram + bacteria. (cannot penetrate outer lipid membrane of Grm _

91
Q

What are the side effects of Vanc?

A

Nephrotoxic, ototoxic, red man syndrome, neutropenia, thrombocytopenia

92
Q

What is the mechanism of resistant to Vanc in VRE?

A

Changeing pentapeptide side chain from D-ala D-ala to D-ala D-lac preventing vencomycin binding

93
Q

What are the resistance genes against vancomycin?

A

VanA, Vanc and teicoplanin resistance - transferable by plasmids
VanB, Vanc R but teicoplanin S, genes on transposon - transferable
VanC low level VANC resistance, Teico S, Not transferable

94
Q

What is transformation in regards to antimicrobial resistance?

A

Acquisition of genetic material from other bacteria in close proximity

95
Q

What is the MoA of macrolidess?

A

They insert into a pocket of the 23S subunit of the 50S ribosome, blocking protein assemply of transpeptidase enzyme.

96
Q

What are the genes responsible for pneumococcal macrolide resistance?

A

mefA or ermB genes

97
Q

What are the eschappm organisms?

A

Enterobacter
Serratia marcescens
Citrobacter freundii
Hafnia alvei
Acinetobacter and Aeromonas
Proteus vulgaris
Providencia
Morganella Morganii

98
Q

What are the carbapenem resistance enterobacteriaeceae?

A

Kleb pneumo carbapenem (KPC)
New Dehli Metallo betalactamase (NDM)
Oxacillin type beta lactamase 48 OXA48

99
Q

How do you treat carbapenemase producing bugs?

A

Colistin, high dose tigecycline, aminoglycosides, fosfomycin, aztreonam

100
Q

What is the MoA of Avibactam?

A

Binds to beta-lactamase enzyme and inactivates it through reversible cyclisation , dosent work against metalo-betalactamses however

101
Q

What is the MoA of amphoterecin B?

A

Polyene - inserts into the fungal membrane

102
Q

What is the MoA of echinocandins?

A

Inhibit glucan synthesis

103
Q

What causes allergy cross reactivity in penicillin and cephalosporin?

A

Shares R1 side chain with penicllin - cross reactivity between amox and cefaclor

104
Q

What is the MoA of aminoglycosides?

A

Binding to the aminoacyl site of 16S ribosomal RNA within the 30S ribosomal subunit, leading to misreading of the genetic code and inhibition of translocation.

105
Q

What is the MoA of Macrolides?

A

Binds to the 50S subunit of bacterial ribosomes leading to inhibition of bacterial protein synthesis

106
Q

What is the MoA of tetracyclines?

A

Reversibly bind the 30S ribosomal subunit blocking protein synthesis

107
Q

What is MoA of fluoroquinolones?

A

Fluoroquinolones act by inhibition of bacterial DNA gyrase. Mutation of this makes them resistant

108
Q

What is the MoA of rifampicin?

A

Rifampicin acts by binding the β-sub-unit RNA polymerase

109
Q

What antibiotic causes urine discolouration (red-orange)

A

Rifampicin/ rufabutin

110
Q

What is the MoA of Daptomycin?

A

Daptomycin binds to bacterial membranes and causes a
rapid depolarisation of membrane potential in both growing and stationary phase
cells. This loss of membrane potential causes inhibition of protein, DNA and
RNA synthesis. This results in bacterial cell death with negligible cell lysis.

111
Q

What is the risk of developing HIV after a needle stick injury from a person with detectable viral load?

A

1:300, 0.3%

112
Q

What is the relative risk of HIV aquisition in men who are circumcised?

A

60% reduction in HIV aquisition ( in hetero men)

113
Q

What host factors confer resistance to HIV?

A

CCR5 D32 homozygotes are resistant to infection.

114
Q

What is one of the main side effects of abacavir?

A

Increased CVD risk

115
Q

What are the side effects of some new INSTI and TAF?

A

Weight gain + metabolic syndrome

116
Q

What do neurominidase inhibitors do?

A

Prevent viral shedding - used in flu

117
Q

What is the mechanism of isoniazid peripheral neuropathy?

A

Vit B6 deficiency

118
Q

What bug? The organism is catalase positive and grows on mannitol salt agar, but does not turn the agar plate yellow. The colonies are gamma hemolytic on sheep blood agar plate

A

S. Epi

119
Q

What is the bad strain of C diff?

A

“hypervirulent” strain, NAP1/BI/027,

120
Q

What is the most important side effect of cidofovir?

A

The most important toxicity of cidofovir is dose-dependent nephrotoxicity; cidofovir has been associated with decreased renal function and the emergence of a Fanconi-type syndrome, with proteinuria, glucosuria, and bicarbonate wasting

121
Q

What mosquito transmits zika?

A

Zika Virus is transmitted by the Aedes mosquito which also transmits Chickengunya and Dengue fever
Daytime bites

122
Q

What is the MoA of aclovir?

A

Acyclovir, a nucleoside analog, is phosphorylated by virally-encoded thymidine kinase and subsequently by cellular enzymes, yielding acyclovir triphosphate, which competitively inhibits viral DNA polymerase
Valaciclovir is a pro-drug

123
Q

What are the MoA of echonicandin, amphotericin and flucytesine?

A

Binds to ergosterol and forms pores: Amphotericin
Inhibits the enzyme that generates beta glucans: Echinocandins (caspofungin - the beta lactams of fungal agents)

Inhibits DNA synthesis: Flucytosine

124
Q

What is the MoA of colistin?

A

binds to lipopolysaccharides on the outer cell membrane of bacteria leading to cell disruption, leakage and death. It is used in cases of carbapenem resistant enterococci with the main side effects of neuro and nephrotoxicity

125
Q

What antibiotic has a large volume of distribution so not good for serious bacteraemia?

A

Tigecycline tissue levels far exceed the serum levels so shouldn’t be used in bacteraemia

126
Q

What are the 2 broad principles for antibiotic killing?

A

Time-dependent (b-lactams)
Concentration-dependent (aminoglycosides)
Toxicity for aminoglycosides is more dependent on total exposure, and killing is dependent on CMAX

127
Q

What are the most common causes of endocarditis?

A

The microbiology is also changing:
- S.Aureus most common then
- Viridans group strep
- Coagulase negative staph
Enterococc

128
Q

What are indications for surgery in IE?

A

IE-associated valve dysfunction complicated by HF, intracardiac abscess, difficult-to-treat pathogen, and/or persistent infection + large vegetations ( 1cm).

129
Q

What are the most common pathogens causing bacterial meningitis in <60 and > 60?

A

<60 - S. Pneumonia, Neisseria meningitisdis, H.influ
>60 - S. Pnuemonia, Listeris monocytogenes, N Meningitidis

130
Q

When should you consider listeria for meningitis?

A

Consider in age >50, those on long term glucocorticoids, immunosuppression, diabetes, alcoholism, cirrhosis, ESRF, malignancy, HIV, transplant

131
Q

What are the CSF findings in listeria?

A

Listeria meningitis can be lymphocytic

132
Q

What are the infection control precaustions for N.Meningitidis?

A

Droplet precaution until > 24h of effective antiboitics.
- Post-exposure prophylaxis for household contacts and health care workers who performed airway management without a mask
○ Rifampicin 600mg po bd for 4 doses Or
○ Ciprofloxacin 500mg po once Or
○ Ceftriaxone 250mg IM once (used for pregnant people)
+/- vaccination

133
Q

What encapsulated bacteria cause serious infection in people with asplenism?

A

S> Pneumoniae, H> Influ type B, N meningitidis

134
Q

What is the mechanism of HSV acyclovir resistance?

A

Tyrosine kinase is needed to activate acyclovir so mutations in TK leads to Acyclovir (and ganciclovir and valganciclovir) being ineffective.

135
Q

What is primary syphillis?

A
  • Shallow, Clean based, painless, rolled, indurated egdes.
  • A solitary, small firm red painless papule on the genital area quickly becomes a painless ulcer with a well-defined margin and an indurated base.
  • Primary chancre
    Heals spontaneously in 7-10 days
136
Q

What is early latent syphillis?

A

acquired within the last 1 years, either known onset of symptoms or have had a negative syphillis test within the last 2 yeas if no evidence of primary or secondary syphillis.

137
Q

What is late latent syphillis?

A

Acquired > 1 years prior to making diagnoisis ( or present with latent syphillis and no previous negative test and no memory of primary syphilis

138
Q

What is sedoncary syphillis?

A

3-6 months after primary chancre - spontaneously resolved, Rash of palms and feet, condylomata lata, lymphadenopathy, constitutional symptoms, mucous pathces

139
Q

What happens in pregnancy if have syphilis?

A

It crosses the placenta at all stages of pregnancy and usually fatal leading to miscarriage

140
Q

How to test for syphilia?

A

If chancre - swab and direct visualisation on microscopy
Serology : Specific treponemal test:
Initially: EIA, FTA, TPHA
These either come back positive or negative. Once positive they stay positive forever.
Then RPR - rapid plasma reagent

141
Q

How to interpret syphilis serology?

A

EIA/CMIA - recombinant antigens - used as screening test as high negatice predictive value. Once positive - positive for life.
If EIA positive then go on to TPPA - specific tremonemal test - to confirm infection ( this is positive by the time develop primary chancre)
TPPA - once positive, always positive.
RPR - non-trepenemal test - indicates disease activity.
It is given as a dilution factor, the higher the dilution factor, the more disease present. a four fold reduction indicates treatment success ( I.e 1:64 –> 1:4)

142
Q

What happens to RPR in pregnancy?

A

Can get false positivei n pregnancy, HIV, SLE and malignancy

143
Q

When do you measure RPR after treatment for syphilis?

A

Four-fold decrease within 6-12 months
Early syphillis: monitor 6 and 12 months
Late syphilis: Monitor 6, 12, 24 months
If RPR titre increases after treatment - the most likely reason is REINFECTION

144
Q

What is the rates of penicillin allergy over time?

A

50% of people who have a penicillin skin test allergy will lose this at 5 years, 80% at 10 years.
The decline in rates of cephalosporin allergy are similar.

145
Q

What is the typical presentation of SJS?

A

Latency of 4-28 days, feverm exanthematous eruption,, prodorome common, mortalisy ~20%

146
Q

What is the typical presentation for DRESS?

A

Latency 14-18 days, rash, fever, +/- prodrome, usually >50% body involvement, facial oedema, renal and liver involvement.

147
Q

What is the spreading pattern for measles rash?

A

Starting on head and descends

148
Q

What bugs are viridans group strep?

A

Strep.Bovis/ S.Gallaplyticus
S.Mutans
S.Sanguinis
S. Mitis

149
Q

What are HACEK organisms?

A

Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species

150
Q

Why do HACEK organisms matter?

A

They can cause culture negative endocarditis

FRACP Exam (15 decks)

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