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1
Q

Describe malaria types, lifecycle, features, diagnosis, chemoprophylaxis, and management

A

Lifecycle- infected anopheles injects sporozoites-> merozoites-> schizonts

Types- falciparum IP 1-4 weeks, causes cerebral malaria, shock and renal failure

  1. P malaria - persists in blood for over 20 years (no hypnozoites),
  2. Vivax- hypozoites, relapses
  3. Ovale - hypnozoites
  4. Knowlesi- zoonotic malaria mainly SE Asia .

Diagnosis- thick and thin film. Need 3 total negative to exclude .
False negatives occur if partially treated
ICT high specificity and sensitivity but doesn’t tell burden of disease.
Severe parasetemia over 2% in all except knowlsi is over 1%

Prophylaxis- doxycycline, mefloquine (contraindicated in neuropsy disorders, cardiac conduction defect), atorvaquone and proguanil

Mx- uncomplicated artemether and lumefantine (Riomet), quinine/doxycycline, atorvaquine+praguanil
If due to vivax and ovale- rest

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2
Q

Describe presentation, complications and management of typhoid fever

A

IP of 1-2 weeks, constipation, fever, hepatosplemeegaly, neuropsychiatric dc, relative bradycardia, rose spots (faint salmon coloured)

Complications- liver or spleen abscess, intestinal obstruction, endocarditis, bone and joint infection esp if grafts

Diagnosis- bone marrow biopsy lost sensitive

Mx- azithromycin, cipro, cef . If severe give sex
Chronic carriers have increased risk of gallbladder cancer

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3
Q

Dengue investigations

What’s its IP

A

Most specific is IgM but takes over 5 data, use NS1 antigen initially . Also seen pancytopenia
Critical to note IP of -10 days

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4
Q

Cause, intestinal and extraintestinal features of amoebiasis

A

Causes by entamoeba histolytica
Presents with dysentery, colitis, toxic megacolon, colonic lesions
Extracolonic are liver/brain/lung abscess , genitourinary diseaee

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5
Q

Diseases that scrub typhus cause

A

Rickettiosis, spotted fever and Rocky Mountain fever . Transmitted by anthropoid
Presents with sudden shakes, fevers, severe headache and Eschar

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6
Q

Describe meliodosis- cause, features, risks, diagnosis and management

A

Caused by burkholderia paeudomalle by inoculation
Most have underlying chronic infection like DM, outdoor or ATSI

Presents acute cases with upper lobe pneumonia . Subacutely with visceral abscess, OM, soft tissue abscess
Diagnosed on any culture of organism

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7
Q

How does schistosomiasis present and it’s diagnosis and management

A

3 phase- migratory phase which is swimmers itch
Acute phase aka katayama fever - eosinophils, hepatomegaly
Need to demonstrate worms in egg or poo
Mx- praziquantel

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8
Q

Describe leptospirosis it’s features, diagnosis and management

A

Febrile illness assoc with flooding , rats are main reservoirs
Features- conjunctival suffusion, jaundice, ARF, pulmonary haemorrhage, Weil’s disease (jaundice and ARF), leptospirosis pulmonary haemorrhage, mengintis, uveitis
Diagnosis- dark field urine exam, PCR, cultures
Mx- penicillin

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9
Q

Describe measles- infective period, complications and Ix and complications

A

Contagious for 5 days before rash appears
Prodtome of koplik spots, conjunctivitis then red maculopapular rash in face and spreading down
Ix- serum measles Ig, NP swan for culture.
Mx- Vit A, supportive , NEGATIVE pressure room (also for TH, VZV)
Complications- ADEM, SSPE

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10
Q

Hepatitis A and E presentation

A

Self limiting but highly contagious. Faecal oral. HepE can be severe in pregnancy

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11
Q

Main cause of travellers diarrhoea

Causes of acute and chronic travellers diarrhoea

A

ETEC in most cases

In acute watery- rotavirus most common in kids and norovirus most common in adults) Bloody diarrhoea EHEC, shigella, salmonella
Shortest IP for staph aureus then bacillus. Guardia takes 1-2 weeks- mx with metro or inidazole

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12
Q

Prevention advise and complications of Zika virus

A

Complications inc neurological like GBS, micro encephalopathy
Prevention- for male 6 months as per WHO (some say 3) and 2 for women - use contraception

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13
Q

Describe how Lyme diseaee presents , cause, and major cause of death

A

Caused
By borrelia burgdorferi spread by ticks
Classical erythema chronic migrans (bulls eye) rash is itself diagnostic . Mx- doxy

Cause of death many cases heart block

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14
Q

Describe how influenza presents and basis if its medications , distinguish causes of pandemics and epidemics , who is suitable for post exposure prophylaxis and the highest risk groups

A

Main antigens are haemaglutinin which binds to body’s surfaces and neuraminidase which cleaves the virus allowing to be unleashed into host

Mx options are neuraminidase inhibitors (1st kind being oseltamivir, 2nd line zanamivir). M2 inhibitors used for influenza A only- they include amatidine and rimantadine
New drug boloxavir is a selective inhibitor of endonuclease which blocks influenza proliferation by blocking mRNA

Treatment should be within 48 hours or if severe within 4 days

Antigenic shift cause pandemics (due to genetic reassortment- only influenza A causes pandemics) whilst antigenic drift cause epidemics due to point mutations in HA and NA

Highest risk in first two trimesters of pregnancy and obesity

Post exposure prophylaxis only for long term care facilities, HIV/HSCT, pregnant

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15
Q

If TB in patient in flight , who would you screen

A

If flight more than 8 hours and within 2 rows of affected patient

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16
Q

Most common extrapulmonary site of TB

A

TB lymphadenitis

Extra pulmonary TB not infection risk

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17
Q

Investigations for TB

A

Need 3 sputum specimens at least 8 hours apart inc at least one early morning specimen for AFB, and mycobacterium culture
Diagnosis established by isolation of the bacteria from sputum/BAL/tissue/pleural fluid OR Positive PCR (NAA)
Note AFB smear alone inadequate

For latent we do so tuberculin skin test and interferon gamma release assay aka quantiferon. IFNgamma tests for cytokine released by TB sensitised WBCs
Note these only test for TB exposure- can not exclude disease or latency in their absence, and can not diagnose latent vs active in their presence
TSST looks at IFN released by T cells, type 4 hypersensitivity. If BCG vaccinated need to be over to diagnosis, in close contacts over 5mm adequate and in patients with RFs over 10mm needed

It has lower specificity to quantiferon if BCG vaccinated.

If pleural or pericardial TB- need tissue diagnosis

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18
Q

Management of standard TB as well as MDR, XDR
And SE of treatment
Mx of latent TB

A

Std is isoniazid, rifampicin, ethambutol, pyrazinamine for pulmonaryband extrapulmonary TB
For latent- isoniazid OR rifampicin

If isoniazid resistant- 2 months of above and 7 months of above except isoniazid

If MDR- means resistant to at least isoniazid and rifampicin - bedaquiline, quinolone, linezolid for 18-20 months.

Note rifampicin resistance is highly predictive of MDR

If XDR- resistant to rifampicin, quinolone AND an injectible (these are kanamycin, amikacin)

Steroids used for TH meningitis/pericarditis and IRIS
IF TB meningitis- mozifloxacin used instead of ethambutol due to better CSF penetration.

SE of antiTB meds- ethambutol causes optic neuropathy and vision loss and high ALT
Isoniazid causes hepatitis, rash, neuropathy (due to increased excretion of pyridoxine/B6- thus give with it )
Pyrazinamixe- main cause of drug induced hepatitis

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19
Q

Most common NTM in Aus

A

MAC

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20
Q

If screened positive for TB and about to start TNFa for RA what do you do?

A

Give isoniazid for 1 months then start TNFa

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21
Q

Main causes of meningitis in young adults and elderly

A

Young adults- neisseria meninitis (gram neg diplococci) then strep pneumonia (gram pos diplococci)

In elderly- strep pneumonia then neisseria then listeria (gram pos bacilli)
Post head injury- pseudomonas, acinobactet, strep, MRSA

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22
Q

Commonest viral cause of meningitis

A

Enterocirus inc coxsacxhie and polio

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23
Q

CSF in viral vs TB/cryptococcal/fungal

A

Viral shows normal sugars and high protein with high lymphocytes

TB/cryptococcal/TB shows high lymphocytes and low glucose

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24
Q

Empirical management of TB

A

Dex within 30 mins and ceftriaxone

If over 50 yrs OR pregnant OR low immunity OR high alcohol= ceftriaxone AND benpen

If neurosurg or head injury= vanc and cefepime/ceftazidine

If suspecting strep pneumo as cause based on pneumococcal antigen positive, suspected OM/sinusitis, gram pos diplococci in stain= vanc, cef and dex

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25
Q

Describe directed therapy in the case of N meningitis, strep pneumo, listeria, GBS, Hib

A

N meningitis= benpen If susceptible otherwise ceftriaxone

Strep pneumo= cont dex, until MIC returns cont cef and vanc. If MIC <0.125 - benpen . If 0.125-1= cef 
If over 1= cef AND vanc or moxiflocacin 
Listeria- benpen
GBS- benpen 
Hib- benpen or cef 
If penicillin allergy vanc and cipro
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26
Q

Presentation and management of cryptococcal meningitis

A

In immunocompromksed due to neoformans in normal gathi
Causes cerebral lesions
Mx- induction with amphotericin AND flucytosine - then continue flucanazole

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27
Q

Cause of esoniphilic meningitis

A

Angiostrongyloids and gnathostoma- mx corticosteroids and anthelmintic

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28
Q

Cause of Mallaret syndrome and its management

A

It’s reccurrent benign lymphocytic meningitis

Caused by HSV2 . Mx- mostly none. If needed oral valaciclovir

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29
Q

Cause of HSV encephalitis and treatment

A

HSV1

IV aciclovir

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30
Q

When is chemo prophylaxis indicated and what do you give

A

Indicated if close household contact with meningitis (over 8 hours within 7 days prior to sx)- single dose cipro. If pregnant- IM ceftriaxone
Only need to give prophecies for N meningitis (and serious HiB)

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31
Q

If a male presents with recurrent meningitis but CH50 normal what’s cause

A

Properidin deficiency (X linked - properin needed to stabilise C3 concertise in alternate pathway)

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32
Q

What’s a unique feature of listeria meningitis

A

Presents in immunocompromosed and with neuro sx like seizures and strokes and palsies

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33
Q

Why do we give dex in meningitis

A

As strep pneumo causes hearing loss and neurological complications and to reduce mortality

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34
Q

List the minor and major dukes criteria for infective endocarditis

A

Major is 2 positive blood cultures with typical organisms
Persistent bacterimia
Positive serology for coxielle (Q fever)
Positive echo (vegetation, abscess, new regurg)

Minor are
Predisposing heart disease or IVDU
Fever over 38
Vascular or immunological phenomenon
Microbiological evidence not fitting major criteria
Definitive IE needs 2 major and 1 minor and 5 minor

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35
Q

What’s the most common valvular lesion in IE

A

MVP

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36
Q

Empiric Management of native and prosthetic valve IE inc typical organisms for each

A

For native- suspect staph then strep viridens, coag neg staph, enterococcus, strep Bovis, HACEK
MX= benpen, fluclox and gent

Prosthetic calicoes- in first 2 months after prosthesis, coag neg organisms most common (skin), and after that same as native bugs
MX= Fluclox, vanc, gent

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37
Q

Directed therapy for strep viridens, staph aureus, HACEK, Q fever

A

Strep viridens - benpen and gent (or benpen for 4 weeks)

MSSA- fluclox
MRSA- vanc +/-fusidix acid

Enterococcus- gent and ampicillin
Q fever- doxy, rifampicin and hydrochloromine

HÁČEK- amoxicillin or benpen

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38
Q

Complications post IE

A

Heart failure secondary to AR/MR leading to cardiogrnic shock, embolisatipn, perianular extension of infection (MONITOR ECG for worsening heart block), splenic abscess and mycotic aneurysm

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39
Q

Endocarditis prophylaxis

What’re the high risk procedures and high risk conditions needing prophylaxis

A

High risk conditions- prosthetic heart valve, prior IE, cardiac transplant with subsequent development of cardiac valvulopathy, congenital heart disease IF it involved an unrepaired cyanosis defect or repaired defect with prosthetic material

High risk procedures are dental extraction/implants/existing disease, resp: invasive ENT/resp tract procedure
GIT/genitourinary- IF abscess, obstruction or infection

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40
Q

Class I indications for surgery in IE

A

Valve stenosis/regular causing heart failure
AR/MR with raised LVEDP
Fungal organisms, heart block/abscess, prosthetic valve endocarditis

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41
Q

Definition, causes and management of culture negative endocarditis

A

3 neg BCs after 7 days- due to fastidious organisms like Q fever etc. if post dental- think strep family

Mx with combination of vanc and ceftriaxone

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42
Q

Diagnostic criteria for ARF

A

Preceding GAS 2-4 weeks before with 2 major and 2 minor JONES

Major= JONES= Migratory polyarthritis, oslers nodes, syndenham chorea, erythema marginatum , subcutaneous nodules

Minor criteri= LEAF mnemonic = Long PR, Elevated ESR, Arthralgia, Fever

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43
Q

Commonest valvular lesion in RHD

A

Mitral regurg which progresses to MS

More likely if carditis occurred during ARF

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44
Q

Other than rhd, what’s another sequele of ARF

A

Jaccoud arthropathy- loosening and lengthening of periarticular tendons in hands, feet

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45
Q

Management of ARF

A

Benzathine penicillin

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46
Q

Secondary prophylaxis post ARF or RHD

A

If no RHD- prevent GAS giving benzathine penicillin for min 10 years or until 2- yrs (whichever is longer)
If developed moderate RHD- continue till 35 years
If severe- 40 yrs
If cardiac surg- lifelong

Annual yearly dental check for all ARF

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47
Q

Describe presentation and management of buruli ulcer

A

Chronic disease due I mycobacterium ulcerans- affects bone and skin. Starts as painless nodule or diffuse painless swelling
Mx- rifampicin and either clarithromycin/moxifloxacin

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48
Q

What syndrome does gonorrhoea cause

A

Fitz Hugh Cuits syndrome

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49
Q

Describe the phases of presentation of syphilis , diagnosis and issues with diagnostic tests

A

Chancre is painless punched out ulcer
Secondary syphilis is seen 6-8 weeks post in half, where macupapular rash develops on face/palm/soles, condylomata., fever
Latent syphilis- patient asymptomatic but blood tests positive. Most diagnosed here.
Tertiary syphilis due to immune destruction with tissue harbouring - inc aortic incompetence due to aneurysm, meningovascular syphilis

Diagnosis - nontreponemal(cardiolipin) inc RPR and VDRL, and if positive then treponemal (TPPA). Once a positive treponemal it remains positive for life- thus not used to monitor progress or detect repeat infection.
Both tests can be negative early on
Non treponemal takes 3 years to disappear after treatment . BUT if the RPR titre rises 4 fold post during this time, it suggests re-infection
Causes of false positive nontreponemal tests- APPS, SLE, HIV, TB

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50
Q

Types and presentation of vaginitis

A

Candida - with OCP, steroids, abx. White cheesy discharges and itch . Acidic.
Mx with fungal pessary and oral clotrimazole
Trichomonas are mostly STI, offensive vaginal discharge - mx metronidazole
Bacterial vaginitis is in sexually actively women fishy greenish thin vaginal discharge . Acidic, diagnoses on whiff test and clue cells seek

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51
Q

List the roles of each of the 5 key antiherpes drugs and their major SE

A
  1. Acyclovir- to treat HSV and VZV. IV prep goes to CNS (thus first line in HSV encephalitis). SE- Nephrotoxicity
  2. Cidofovir- for CMV retinitis in HIV infected patients. SE: neohrotoxicity
  3. Ganciclovir- IV ganciclovir (or its oral prodrug valganciclovir) for active CMV
  4. vanganciclovir is main agent for CMV prophylaxis in solid organ transplant and stem cell when used
    Oral valganciclovir is converted to ganciclovir.
    SE- bone marrow suppression
  5. Valacyclovir- treats genital herpes and VZV. Can be used for prophylaxis against RENAL transplant against CMV
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52
Q

Describe role of antiviral prophylaxis in the two types of transplants

A

All solid organ transplants with either donor or receipient CMV pos gets valganciclovir prophylaxis (if CMV for both negative we give valacyclovir for HSV prophylaxis without testing )
If haem stem cell transplant- monitor routinely to see if patient develops CMV PCR positive to avoid marrow suppression

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53
Q

List the steps of HIV invasion

A

Binding/attachment to CD4 receptor

Fusion (HIV envelopes CD4)

Reverse transcription (HIV’s reverse transcriptase converts its RNA to DNA and enters our CD4 nucleus)

Integration - HIVs integrase allows viral DNA to integrate into CD4

Replication

Assembly

Budding- by HIV proteases

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54
Q

WHO stages of HIV

A

Primary HIV, clinical stage 1 (persistent generalised lymphadenopathy), stage 2 (weight loss of under 10%), stage 3 (weight loss over 10%, oral candidiases, oral hairy leukaemia), stage 4 is HIV wasting syndrome

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55
Q

Diagnostic tests for HIV

A

Antigen p24 year
HIV ELISA (combined Ag/Ab test)
HIV viral load for monitoring
Also do genotype testing baseline for all

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56
Q

Main cause of death in treated HIV

A

Non aids malignancy then CVD

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57
Q

What’re the management options in HIV

What’re their key SEs

A

Start for all

NRTI- tenofovir, lamivudine, abacavir,
SE- mitochondrial toxicity presenting as peripheral neuropathy, pancreatitis , lipoatrophy (subcut fat wasting), hepatic steatosis, lactic acidosis
Tenofovir causes Fanconi syndrome and ATN and low BMD
Abacavir causes hypersensitivity with fever/malaise

NNRTI- etavirenz
SE- vivid dreams, rash, teratogenic

Protease inhibitor- ritonavir

Integrase inhibitor- raltegravir, dolutegravir

Most on 2NRTI and an integrase inhibitor

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58
Q

Management of HIV and hepB coinfection

A

Tenofovir, embricitabine

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59
Q

Why do we add low dose ritonovir

A

To increase ART potency, improves its pharmacokinetics (and reduce pull burden)

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60
Q

What’s a critical test before starting abacacir and why

A

HLA5701 to reduce risk of abacavir hypersensitivity (need to wait for this)

61
Q

Which ART increase CVS risk

A

Abacavir and protease inhibitors

62
Q

Define treatment success in HIV

A

Viral load suppression is goal- under 200

63
Q

Define virological failure and virological rebound in HIV

A

Failure is when HIV RNA is above 200 after 24 weeks on ART

Virological rebound is repeat detection over 200 after suppression

64
Q

What do you do if drug resistance suspected and likely cause

A

Most due to noncompliance, do genotype testing again

65
Q

Drugs to avoid with ritonavir

A

Ritonovir is P450 inhibitor- don’t give simvastatin or lovastatin (causes rhabdo) or Midaz (increases sedation)

Tenofovir and ritonovir both relatively c/I in TB patients due to interactions with rifampicin

66
Q

Who gets preexposure prophylaxis for HIV and with what

A

High risk like MSM, transgender, partner HIV pos

Tenofovir and embricitabine

67
Q

When and what to give as post exposure prophylaxis

A

2 drugs if source HIV status unknown but anal sex with MSM or high prevalence country
3 drugs if source HIV positive with unknown viral load or high viral load (if suppressed VL- no treatment!)
If needle stick in health care worker- treat whilst awaiting results, or source cannot be identified continue PEP in high risk situations .

Start within 1-2 hours, no point after 72 hours

68
Q

How to manage a pregnant woman on ART for HIV

A

Maternal CD4 over 500 confers lowest risk of transmission
If mum is HIV infected- continue ART
If pre delivery material VL inadequate or unknown give intrapartum zidovudine. And give baby ART within 6 hours and continue for 4 weeks
C section only if VL over 400 at 36 weeks. Breastfeed if good VL

69
Q

What’re the only situations where we don’t start ART in HIV

A

If cryptococcal meningitis, CNS TOXO, TB meningitis as higher risk of ITIS and in CNS infections no place for inflammatory markers to go

70
Q

When to start ART in TB -HIV patient

A

If TB AND CD4 over 50- don’t start ART for 4-8 weeks of TB treatment
If TB and CD4 under 50- ART at 2-4 weeks

71
Q

When do we suspect MAC and what do we give as prophylaxis in HIV patients

A

Once CD4 under 50 give azithromycin

72
Q

CNS mass lrsions in AIDS

A

Toxo, primary CNS lymphoma, PML, TB

73
Q

What’re AIDS defining malignancies

A

NHL, kaposi’s sarcoma, cervical cancer and cryptococcal infections

74
Q

Describe HIV-associated neurocognitive disorders (HAND)

A

Prev called HIV encephalitis - marked by subcortical dysfunction (unlike AD) with reduced attention, concentration , depression, memory)

75
Q

Of those hospitalised pneumonia’s commonest cause

A

Pseudomonas aeroginosa (gram neg bacilli)

76
Q

What’re the extra hepatic manifestations of hep C

A

Mixed cryoglobuliemia , DM in 70%, NHL, MALT, lichen planus, thyroid dysfunction, Sjogrens

77
Q

Diagnosis for HCV

A

1st do HCV Ab, if pos do HCV PCR (confirms active infection) and if positive viral load and genotype testing in all

78
Q

What’s quasispecies and implications

A

Quasispecies is presence of different strains in infected host
Causes viral persistence, reduced response to IFN, harder to develop vaccines

79
Q

Main cause of cirrhosis in Aus

A

Hep C

80
Q

Management of hepatitis C

A

All

Options are
1. NS3/4A- protease inhibitors (high risk of resistance thus not used alone). End in “previr”

NS5A end in “avir”

NS5B end in “buvir”

Combo options are
12 weeks of sofosbuvir and velpatasvir
Alternative is 8 weeks of glecaprevir and pibrentasvir (give for 12 weeks if cirrhosis, 8 weeks otherwise)

81
Q

Which drugs are contraindicated with DAA

A

Amiodarone (causes heart block) and carbamazepine

82
Q

Which drug contraindicated in renal failure

A

Cannot use sofosbuvir when GFR under 30

83
Q

How to manage hep C in pregnancy y

A

Ideal to avoid for 6 months before and after
Very low perinatal transmission
If mum is positive test baby at 15-18 months

84
Q

Management of treatment resistant hep C

A

These likely have resistance and need triple therapy

Sofosbuvir, velparasvir and voxillaprevir

85
Q

Post exposure prophylaxis for hep C

A

Usually none!
If source is HCV At and Ab positive AND detectable viral load- test patients HCV Ab and viral load immediately, 2 months and 6 months and if positive then treat

86
Q

Phases of hep B disease

A

Phase 1 is immune tolerance and phase 2 is immune clearance (eAg positive in both, starting to become eAb positive)

Phase 3 is immune control and phase 4 is immune escape

87
Q

Interpret cause

HBsAg positive, HBeAg neg, HBeAb positive

A

Inactive carrier

88
Q

Interpret

In known HEP B there’s an increase in HBV DNA and ALT

A

Deactivation

89
Q

Interpret

HBsAg neg, HBsAb neg, HBcAb pos

A

Infection resolved long time ago (most likely)

Recovering from acute (time between sAg loss and sAb development)

Passive transfer in kids

False positive result

Occult HBV! (Need viral load done to confirm)

90
Q

Interpret

HBsAg neg, HBsAb pos and HBcAb pos

A

Immune due to infection (recovered)

91
Q

Interpret

HBsAg neg, HBsAb pos, HBcAb neg

A

Immunised

92
Q

Interpret

HBsAg pos, HBsAb neg, HBcAb pos , HBcIgM Ab pos

A

Active infection (sAg was ages 3-4 months to disappear- if remains chronic infection)

93
Q

Interpret

HBsAg pos, HBsAb neg, HBcAb pos, HBcIgM neg

A

Chronic infection

94
Q

What’s pre-core mutant, core mutants

A

PreCore mutant production of HBeAg positive but preserves
HBcAb

Core mutant is reduced HBeAg but unregulated HBcAb

Suspect as cause when eAg neg but high viral DNA load and high ALT

95
Q

How does occult HBV present

A

Absent HBsAg but HBV DNA present

Same risk of cirrhosis as nonoccult infections

96
Q

Post exposure prophylaxis in hep B

A

If vaccinated and known responder- Nil

If known non responder - if source neg then nill, but if source pos or unknown give HB immunoglobulin and follow up for seroconversion

If source HBsAg over 10- treat as responder and no treatment

97
Q

If HbsAg pos and about to start ritux what do you do

A

Give prophylactic lamivudine or entacavir immediately and continue for 6 weeks post cessation of immunisation

Some even treat if sAb pos and cAb pos even if sAg neg as can still reactivate

98
Q

WHen do we treat Hep B

A

If HBV DNA over 2000 AMD ALT high with biopsy showing moderate fibrosis

If HBV DNA over 20,000 and ALT twice the ULN

Compensated cirrhosis, particulate if HBV DNA over 2000

All decompensated cirrhosis

99
Q

Best time to treat

A

Immune clearance and escape phases (where highest risk of cirrhosis)

100
Q

Three options for management of Hep B

A

Nucleoside analogues - entecavir, lamivudine (high resistance) , telbivudine

Nucleotide analogues- tenofovir,

Cytokines - pegylated infterferon - cannot use if decompensated liver

101
Q

If hep b induced decompesated cirrhosis how to manage

A

Use combination of nucleoside and nucleotide

102
Q

Management of hep B and C coinfection

A

Tenofovir and lamivudine

103
Q

Management of Hep B in pregnancy

A

Avoid even if in treatment
If have to use (high viral load esp eAg pos) use tenofovir or lamivudine in 3rd trimester
All infants born to mothers of HBsAg pos should get HBIG within 12 hours and be vaccinated

104
Q

WHich of hep B or C cause cancer and which cause transmission after needle stick

A

Both Hep B

105
Q

Describe Hep D

A

RNA virus that coinfection with hep B , HBV DNA is low in chronic HDV as HDV suppresses the HBV

Compared to coinfection (when both occur at same time) if HDV in setting of chronic HBV more likely liver failure

106
Q

Most aggressive virus causing hepatitis

A

Hep D

107
Q

Management of Hep D

A

Pigialated interferon alpha for at at least 48 weeks , most relapse
Transplant only cure

108
Q

Main cause of Hep E

A

Pig meat

Mostly in immunocompromoser

109
Q

Gram positive (purple) bugs can be classified into cocci and bacilli/rods

A

Cocci- catalase positive are subdivided into coagulase positive (staph aureus) and coag neg staph epi (form biofilm)

Catalyse neg form alpha (strep viridens), beta (GAS, group b is strep agalactrae, Strep bovis (causes endocarditis and colon cancer)

Entercocci - all intrinsically resistant to cephalosporins- faecalis (penicillin susceptible, not virulent) and fascium (bad, most VRE)

Bacilli/rods inc clostridium, bascillus, listeria (intrinsically resistant to cephalosporins), Nocardia (pos modified acid fast)

110
Q 
Gram negatives (pink) divided into cocci and bacilli/rods 
List them
A

Cocci- neisseria

Bacilli inc enterics (E coli, Klebsiella which are intrinsically resistant to amoxicilllin, proteas, campylobacter , shigella, vibrio cholera), fastidious (haemophilus, legionella, Morexella, HACEK which are mx with ceftriaxone ), environmental (like pseudomonas, burkholderia), ESCAPPM (inc enterobacter which are inducible to 3rd gen cephalosporins)

111
Q

What’re the atypical

A

Chlamydia, coxiella brunetti, rickettsia, mycoplasma, spirochittes like treponemal

112
Q

Which bugs are intrinsically resistant to cephalosporins

And amoxicillin

A

Resistant to amoxicillin with klebsiella

Listeria and all enterococcus are resistant to cephalosporins

113
Q

What antibiotics are community or nmMRSA sensitive to

A

Vanc, Bactrim, clindamycin

114
Q

List the 7 groups of drugs under beta lactams

A

Penicillin (benpen, piptaz etc), cephalosporin, beta lactamase inhivitors, cephalosporin, vanc, teicoplanin, carbopenem, and monobactams (aztreonem)

115
Q

Distinguish between Aug and piptaz in what they cover

A

Both cover gram hey and entero and anaerobes but piptaz also covers psuedomonas

116
Q

What happens to the coverages of cephalosporins as we progress generations

A

We lose gram pos and gain gram neg cover

117
Q

How’s teicoplanin different to vanc

A

Both glycopeptides but teicoplanin also covers VRE-VanB

118
Q

DIfference between meropenem and entapenem

A

Both carbopenems covering ESBL, but ertapenem is once daily dose but has no pseudomonas cover

119
Q

Which beta lactam doesn’t need renal adjustment

A

Cephalosporins

120
Q

How is the killing different between beta lactams and aminoglycosies

A

Beta lactams kill based on time above MIC, aminoglycosides kill on AUC/max conc

121
Q

List the 5 protein synthesis inhibitors and their subclasses

A

Aminoglycosides (gent, tobramycin, streptomycin), tetracyclines (doxy), macrolide (inc azithromycin, erythromycin, clarithromycin), linocosamide (clindamycin), linezolid

122
Q

List the two DNA synthesis inhibitors and their subclasses

A

Fluroquinilions (cipro and moxi) and metro

123
Q

Main SEs with fluroquinilones

A

QT pronlgation, tendon rupture, retinal detachment , strong association with C diff

124
Q

Main indication got amikacin

A

CPE

125
Q

List the 4 major mechanisms antibiotics use for resistance and list examples

A
  1. Antibiotic inactivation- haemophilus, staph, ESCAPM, ESBL, beta lactamases
  2. Alteration of antibiotic target sites - such as PBP sites - strep pneumonia, coag neg strep, MRSA, N meningitis
  3. Decreased permeability - seen in enterobactera, psuedomonas to trimethoprim, vanc and sulphonamides
  4. Antibiotic efflux- seen with pseudomonas, linezolid
126
Q

What’re the virulence determinants in nmMRSA

A

Panton Valentine leukocidin (causes WBC destruction and tissue necrosis) - causes skin and soft tissue infections

Alpha hemolysin, phenol soluble modulator

127
Q

Distinguish VISA vs VRSA

A

Both MRSA but VRSA are not susceptible e to vanc (MIC over 16)

VISA mainly seen in dialysis patients or those with infected foreign bodies receiving frequent vanc- associated with thickener cell wall .
VRSA - associated with van genes from VRE

Mx- linezolid (DAPTO DOES NOT WORK)

ASSUME when MRSA patients don’t get better on vanc

128
Q

What antibiotic has been a risk for VRE

A

Metro used in aspiration pneumonia symptoms

129
Q

Which Abx use increase ESBL risk

A

Fluroquinilones

130
Q

Which bacteria mainly cause ESBL

A

Klebsiella but also R coli, salmonella etc

131
Q

Two types of CPE and their management

A

Klebsiella pneumonia CPE- mx ceftazidine-avabactam, colistin-polymixin

Metallobetalactamase- aztreonam and colistin

132
Q

Type A vs Type B ADR

A

TYpe A is non immune

Type B is T cell or IgE mediated hypersensitivity

133
Q

Of the cephalosporins which is safest in penicillin allergic patients

A

Cefazolin as no common side R chain

134
Q

MAangement of different types of osteomyelitis

A

If long bone- fluclox

If vertebral - ceftriaxone and vanc

135
Q

Management of two types of necrotising fasciitis

A

Type 1 involves poly microbes whilst T2 is mainly GAS

MX- surgical exploration, meropenem, clindamycin and Vanc, and IVIG suspected

136
Q

What’re the 3 phases post transplant and which organisms predominate in each

A

In preengraftment phase - mostly bacteria and candida

In post engraftment it’s CMV, BK, fungi

Phase 3 is late phase where we see encapsulated bacteria, CMV, VZV, pneumocystis

137
Q

Commonest infections after solid organ transplant under 1 month, 1-6 months and over 6 months

A

Under 1 month- associated with surgery like MRSA, candida, catheter , wound

In 1-6 months- CMV, HBV, BK, TB

After 6 months- pneumonia, aspergillus, CMV HSV, moulds

138
Q

Commonest infections after solid organ transplant under 1 month, 1-6 months and over 6 months

A

Under 1 month- associated with surgery like MRSA, candida, catheter , wound

In 1-6 months- CMV, HBV, BK, TB

After 6 months- pneumonia, aspergillus, CMV HSV, moulds

139
Q

WHats the new antiviral agent used for CMV prophylaxis

A

Letermovir

140
Q

There are 4 major classes of antifungal agents. List examples of them and their mechanism

A
  1. Azoles- inhibit CYP450 and thus ergosterol which interferes with membrane synthesis
    Inc imidazole group (ketocomazole and clotrimazole) and thiazoles (fluconazole, voriconazole, posaconazole and itraconazole)
  2. Polyenes- inc amphotericin B (new prep is liposomal amphotericin B aka
    ambisome which are also membrane inhibitors
  3. Echinocandins inc capsofungin and
    These inhibit fungal cell wall synthesis
  4. Flucystine
    Inhibit DNA
    synthesis
141
Q

First line management for invasive aspergillosis, candidemia, prophylaxis and cryptococcal meningitis

A

For candida echinocandins used
If stable can use fluconazole too

For cryptococcal- induced with flucystosine and ambisome

For invasive aspergillosis- voriconazole

For prophylaxis- posaconazole

142
Q

MAnagemrn of MAC

A

Clarithromycin/azithromycin, rifampicin, ethambutol

143
Q

Gold standard for pertussis diagnosis

A

Culture from NP is gold standard

144
Q

Gold standard for diagnosis of invasive aspergillosis

A

Galactomannan (cell wall of aspergillus)- more accurate than BAL BUT often we do both

145
Q

In C diff what does a positive culture but negative toxin mean

A

Colonisation

146
Q

Management of meliodosis

A

Ceftazidime , carbopenem

147
Q

What’re the live vaccines

A

BCG, encephalitis, MMRV, zoster, typhoid, yellow fever

148
Q

WHen do you treat an asymptomatic candida UTI

A

If neutropenic or urological procedure

149
Q

How do BK and adenovirus present in renal vs haem transplant

A

Cause tubulointestinal nephritis and urethral stenosis in kidney transplant

In bone marrow transplant cases haemorrhagic cystitis

CLB can cause myelitis and radical it is as well - and with diarrhoea can mimic GVHD (thus biopsy sometimes needed or CMV PCR)

ID Qs (1 decks)

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