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111 Cards in this Set
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IE most associated with CRC |
Strep bovis |
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Empiric treatment for IE (big friendly giant with IE)
Low/high risk of MRSA/sepsis, or prosthetic valve |
Benpen + fluclox + gent
If high MRSA risk or septic, substitute benpen for vanc |
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Empiric AB IE viridans strep or strop bovic Including options for MIC |
Uncomplicated: benpen + gent If MIC >0.125, continue above If <0.125, benpen mono therapy If penicillin allergy, ceftriaxone mono, or vanc mono if severe immediate |
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HIV opportunistic infections by organ (needs revisiting) Brain 7 Gut 2 Lung 4 |
Meningitis/Brain Toxoplasmosis Cryptococcus PML CMV TB Syphilis VZV
Gut CMV ?strongyloides
Lung PJP Aspergillus Cryptococcus TB
Unsure Burkholdaria |
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SBP most common pathologens 2 most common 2 others Which category is uncommon? |
E. Coli + klebsiella most common Less common: strep, enterococci.
Note anaerobics are uncommon |
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Headache and fever differentials apart from standard bacterial/viral meningitis |
Leptospirosis - urine / fresh water / wells - conjunctival suffusion/haemorrhage - in severe cases: hyponatraemia, thrombocytopenia, liver failure, renal failure
Rickettsia - Tick eschar - Resp illness, severe myalgias, lymphadenopathy, prolonged fever (2 weeks) - LFT derangement, thrombocytopenia, relative bradycardia Q fever - Cows/farm animals Malaria / dengue fever Typhoid Septic dural sinus thrombosis - Eye swelling, diplopia, altered mental state |
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Most common cause of viral meningitis vs encephalitis |
Encephalitis HSV1 Meningitis enteroviruses (e.g. coxsaki). When caused by HSV, its HSV2 not 1 |
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Treatment of E. Faecalis IE Fully sensitive And various resistances Penicillin allergy |
Ampicillin 2g 4 hourly (or benpen or amoxy) Plus gentamicin synergy 1mg/kg 8 hourly If gentamicin resistance, substitute gent for ceftriaxone 2g 12 hourly
If penicillin allergy or resistant to amp, use vanc + gent |
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Linezolid Mechanism 1 side effect Spectrum Uses |
Protein synthesis inhibitor (which inhibits toxin production from staph aureus/strep pyogenes like clindamycin) Also is a weak monoamine oxidase inhibutor, so can cause serotonin syndrome Almost all gram + bacteria. Ineffective against all gram negative Used for resistant gram positives like severe nocardia, VRE, MRSA, coag negative staphs |
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Nocardia Genus and defining feature 3 most common organs How to classify as mild, mod, severe Treatment of each of these categories |
Environmental gram + bacilli, forms outbranchings like hyphae (actinobacteria)
Can affect anywhere in many different ways, but most commonly lung, skin and brain abscesses
Mild: immunocompetent non-severe skin Mod: immunocompromised with skin infection, immunocompetent with severe skin, any with mild-mod pneumonia Severe: severe pneumonia, brain involvement or disseminated disease
Mild: bactrim 3 months Mod: bactrim + linezolid 2 weeks, then bactrim 3-12 months Severe: bactrim + linezolid + mero/imipenem/amikacin for 3-6 weeks, then bactrim for 12 months, maybe indefinitely |
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Top 5 bacteria causing pneumonia per study from 2008 |
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Way to grossly categorise streptococci |
Alpha haemolytic (think higher up i.e. mouth and resp tract) Strep pneumoniae. Optochin positive (sensitive to it) Viridens strep Beta haemolytic (think lower down i.e. cellulitis) Strep pyogenes (group A) Strep agalactiae (group B) Strep pneumoniae is the only one that grows in diplococci, but ?can also grow in longer chains |
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Haemophilus influenzae gram stain Resistance |
Gram -ve coccobacillus 40% are ampicillin resistant |
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Doxycycline mechanism |
Inhibits 30s ribosomal subunit |
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Dengue fever Organism Most common travel-related illness from where 4 clinical features 2 major complications 4 laboratory features Diagnosis Management |
Organism Mosquito-borne flavivirus - (Aedes aegypti mosquito) Region
South east Asia / Latin America Clinical features Short incubation period High fever Headache/retro-orbital pain Rash (maculopapular) Arthralgia/myalgia Complications
1. Shock with increased vascular permeability 2. Bleeding from thrombocytopenia/ coagulopathy 2nd time catching it, if from a different one of the 4 strains, may result in worse disease due to cross-reacting antibodies somehow facilitating entry of the virus into cells via the Fc domain Bunch of other rare complications possible
Lab findings Thrombocytopenia Neutropenia Transaminitis Coagulopathy Diagnosis PCR Serology: IgM 3-5, IgG after 7-10 days Management Supportive |
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Hep B test interpretation |
Surface antigen: current infection Surface antibody: immune (whether from immunisation or prev infection) Core antibody: infection at some point (whether resolved or current) - IgM: acute/recent - IgG: past infection or carrier status In someone with positive surface antigen: HBeAg: high infectivity Anti-HBe: low infectivity |
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Caspofungin Main use Other indication sometimes used for Mechanism |
Mainly invasive candidal infections Sometimes used for invasive aspergillosis in combination with other agents Inhibits beta D glucan, which are branched polysaccharides used for crosslinking the cell wall |
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Voriconazole 2 main uses |
Invasive aspergillus Candida |
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2 candida species that fluconazole is not effective against |
C. krusei C. Glabrata Cruisy lab rat |
Cruisy lab rat |
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Invasive aspergillosis management |
IV Voriconazole (preferred) Or IV Amphotericin B
Once clinically improved, switch to oral voriconazole for 6-12 weeks |
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Fluconazole activity |
Yeasts - Candida (but not the cruisy lab rat) - Cryptococcus) |
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Septic arthritis most common organism in young sexually active adults |
Neisseria gonorrhoea |
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C diff lines of tx
1 drug to avoid apart from offending AB Complication |
Oral/IV metro or oral vanc
First recurrence or refractory (3-4 days) first ep Oral vanc or fidaxomicin
2nd recurrence or ongoing despite above Stool transplant If not available, continue vanc/fidaxomicin
Severe Vanc +/- metro
Bezlotoxumab is mentioned in passmed, but etg says role yet defined
Note toxin remains positive for some time after treatment - stop treatment based on symptoms and dont retest for completion
Avoid PPI
Toxic megacolon |
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Whipples disease Cause 2 most common features 2 other |
Tropheryma whipplei (gram + rod) - Ubiquitous but rarely causes disease, when it does it's white Europeans Chronic multisystem disease: - Initially chronic migratory arthralgia - Then chronic diarrhoea/abdo pain, that can lead to malabsorption and wasting Other Cognitive impairment IE |
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Gonorrhoea Micro 2 tests to do Treatment - Empiric - Penicillin susceptible confirmed or where resistance is less common What to do for asymptomatic infection 2 other things to do |
Gram negative diplococci PCR and culture Single ceftriaxone 500mg IM + single oral 1g azithro 3g amoxy once + probenecid + azithro
Treat asymptomatic as above
Contact trace Test for chlamydia, HIV, syphilis |
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HIV transmission risks in order Percentage of MSM with HIV in Australia |
Receptive anal w/ ejaculation: 1/70 Shared needle: 1/125 Receptive anal w/o ejaculation: 1/155 Insertive anal - uncirc 1/160 - circ: 1/900 Receptive vaginal Insertive vaginal Oral unmeasurable 10% |
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PEP post exposure prophylaxis Indications |
For all below, has to be within 72 hours General principle: if risk 1/1000 - 3 drug regimen. If 1/10000 - 2 drug regimen
Known HIV but known undetectable viral load - nil needed (0 transmissions from studies so far) - Only one is occupational needle stick/non intact skin to mucous membrane exposure where 2 drug regimen to be considered (just coz no studies looking at blood born yet)
Known HIV but not on treatment or detectable viral load or unknown - 3 drug regimen for all vaginal/anal sex and needle sharing/needle stick injury and mucous membrane vs non-intact skin - Not recommended for oral sex
Unknown HIV If source MSM or from high prevalence country, give 2 drug therapy for all anal sex and needle injuries/sharing Consider for vaginal if MSM/HPC Not recommended for broken skin/mucous membrane, or for oral sex |
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PEP regimen PrEP regimen |
PEP 28 day course
2 drug - tenofivir + one of emtracitabine or lamivudine (all NRTIs)
3 drug Above + one of - Dolutegrevir - Raltegravir - Rilpivirine
PrEP Tenofovir + emtracitabine daily |
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Other testing to do when someone presents for PEP |
HIV serology + viral load Syphilis serology 3 site STI check (gonorrhoea, chlamydia) Hep B/C Repeat each of above at 4-6w and 3m, except hep B/C which is 3m only |
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PrEP followup bloods |
Baselines HIV serology/viral load Syphilis Hep B/C STI 3 site Renal fx +ACR Every 3 month (90 days) HIV serology, syphilis serology, STI 3 site check Preg test Renal function + urine alb:creat (tenofivir) - only at first 90 days, then 6 monthly Hep C 12 monthly |
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Opportunistic infections at various CD4 counts |
<350: VZV, kaposi sarcoma <250: oral candidiasis, PJP (~200) <150: NHL, cryptococcus, HSV <50: CMV, NTM |
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PJP classic features (3) 1 auscultation feature XR findings 1x complication Management |
Fever, cough, dyspnoea that is significantly exertional Minimal auscultation findings Diffuse consolidation on cxr in the middle (basal/apical sparing)
Pneumothorax
Bactrim - 2nd line: desensitisation, pentamidine, dapsone, atovaquone Steroids if hypoxic |
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Prophylaxis of PJP in HIV - CD4 cut-off for primary, and for secondary |
Primary prophylaxis if CD4 <200 Secondary prophylaxis |
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Cryptococcal meningitis in HIV Presentation Investigations - 3 characteristic findings/Ix of CSF Management |
Headache and fever, slow onset Meningism occurs late Can have behavioural change or confusion Investigations LP - High opening pressure - Positive india ink (circular rings) - CSF crag - WCC/protein/glucose may be normal (glucose low or normal) Mass lesions rarely seen on CT in HIV patients not on therapy, but may be with IRS. But there may be evidence of increased ICP Management Amphotericin + flucytasine then 8 weeks fluconazole Therapeutic LP/shunt |
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Toxoplasmosis in non-HIV Organism Clinical features in non-HIV Key lab finding Diagnosis Management |
Organism Toxoplasma gondii - intracellular protozoan Usual reservoir is cat Clinical features Resembles EBV - fever, sore throat, lymphadenopathy Lag finding Esosinophilia Serology (peaks at 2 months) +/- histo Management Nil unless immunocompromised or severe disease |
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Toxoplasmosis in HIV Usual CD4 count Clinical presentation Investigation |
CD4 count <100 Presentation Usually encephalitis - headache, confusion, neurological deficit, may have fever Extra-cerebral - Pulmonary - Ocular Brain imaging - Ring-enhancing lesions and sometimes mass effect - May appear on CT, but MRI more sensitive |
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What is IRIS in HIV Which infection is particularly implicated |
Description Immune reconstitution inflammatory syndrome Worsening of pre-existing infection, or unnasking of occult infection after commencement of anti retroviral therapy due to sudden immune response Clinical features Onset 1 week - 3 months May result in generalised systemic symptoms (fever, malaise), or specific symptoms of the infection Cryptococcal meningitis Treat with steroids, or delayed anti retroviral therapy |
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Vaccines to avoid in patients on immunosuppression |
Avoid live vaccines in severe immunosuppression e.g. anti tnf and rituximab |
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Management of acute hep B |
Supportive Sometimes consider anti retroviral therapy Sometimes liver transplant indicated |
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TB highest incidence rates |
Sub-Saharan africa and south-east asia |
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Explain TB 'lifecycle' |
Droplet spread into respiratory tract (need prolonged exposure to contract it), then 1 of 3 things 1. TB killed for good 2. Primary infection (5-15%) - Pleural effusion - Miliary TB - CNS TB 3. Latent TB - contained within granulomas - 90% never re activated - 10% reacticate, causing "post-primary" TB, usually when immunosuppression develops (HIV, diabetes, renal failure, immunosuppressive drugs). Most comminly pulmonary TB and most commonly within 5 years of initial TB infection |
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3 things that TB is contained by |
Th cells (hence why so prevalent on HIV) Interferon gamma TNF-alpha |
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2 ways to detect latent TB and their issues/considerations |
Tubucerlin skin test (TST) - Inject BCG under skin and measure induration (not erythema) 48-72 hours later - Measures T cell response to BCG, implying exposure to BCG
Considerations - Not specific for TB - can be activated by NTM - Can also be activated by prev BCG vaccination - The size of induration considered to be a positive result depends on pre-test probability and previous BCG vaccination/Immunsuppression
IGRA (2 types, main one used here is quantiferon gold) - Incubate serum with TB-specific proteins and measure release of interferon in response
General limitations for both of above - Doesnt differentiate between latent and active TB - Reduced response in immunsuppressed patients - Can be false negative in active TV or within 8 weeks of exposure event you're testing for (coz need to wait for T cell adaptive response)
If one of above positive, check for signs of active TB (not sure what this entails but i think just CXR and any clinical signs. ?if these are positive then do 3x induced sputum) I dont know how to differentiate between latent TB and someone who has just treated their TB and retained an adaptive immune response. ?I think they're all just assumed to be latent |
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Diagnosing active TB 3 lab tests and sensitivity 1x investigation |
AFB 65-85% sensitive, increased by 2-5% with subsequent samples so advice for 3 samples Sens is lower in non-sputum samples Quantified from 0-4+ indicating degree of infectivity
PCR/NAA 85% sens, 98% specific Also detects Rifampicin resistance Sens varies by sample type Can detect recently treated TB which isnt necessarily still positive
Culture takes 6-8w CXR
Whole genome sequencing coming soon |
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Latent TB - who to treat 4 options for treatment including duration Main side effect to monitor |
Treat in most people - Immunsuppressed or starting immunosuppression - Healthcare worker - Age less than 35 - Close contact with someone with active TB - Recent conversion to positive of tuberculin skin test 4 options 1. 9 months isoniazid 2. Rifampicin for 4 months 3. Rifampicin + isoniazid for 3 months 4. Rifapentine + isoniazid for 3 months Per lecture, isoniazid preferred in patients undergoing Immunsuppression due to fewer interactions (I think)
Monitor liver function especially isoniazid (hepatocellular per that mnemonic) |
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Active TB treatment Main role for each 1 key side effect of each |
Short course 2 months RHEZ then 4 months RH
Rifampicin - hypersensitivity Isoniazid - peripheral neuropathy Ethambutol - optic neuritis Pyrazinamide - arthritis/gout (Hi Noa)
Hepatitis in all except ethambutol
Prevent resistance: R/isoniazid Early bactericidal: isoniazid Sterilising: rifamp, pyrazinamide
Given by directly observed therapy (DOT) to improve adherence |
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Management of anti TB associated hepatitis |
If less than 5x ULN and asymptomatic, then monitor If not then stop and retrial once at baseline If not working then use alternate regimen |
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TB/HIV treatment timing - which to initiate |
If CD4 <50: early ART with TB tx (does have a risk of IRIS) Exception is for meningitis, where treatment of TB is recommended first
>50 - Tx TB for 8 weeks then ART
Can use pred to prevent if cd4 <100 |
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TB meningitis treatment |
Substitute ethambutol for moxifloxacin 9-12 months Give dex early |
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TB most common causes of treatment failure |
Non compliance |
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Leptospirosis Organism Exposure factor Clinical features (2) 3 organ complications Diagnosis Management |
Organism: spirochaete
Exosure: cat piss in fresh water Clinical features Flu like illness Conjuctival suffusion 3 complications
Aseptic meningitis AKI Hepatitis Diagnosis Serology (but delayed), PCR, blood culture Management Benpen or doxy or ceftriaxone |
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Schistosomiasis Organism 3 species Diagnosis 2 acute manifestations 1 chronic manifestation Treatment |
Flatworm S. Mansoni, s kaponicum, so harmotobium
Katayama fever (acute schistosomiasis syndrome) - Fever - Eosinophila, urticaria, angioedema - Fever - Cough, arthralgia, myalgia - Diarrhoea
Swimmer's itch - Short lived itchy papules
Chronic infection - Bladder calcified lesions
Diagnosis Eggs in stool/urine/biopsy
Treatment Praziquantel (and pred if katayama syndrome) Quatzoquatel vs capernacus, with help of charles manson and toby |
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Febrile neutropenia ABs |
Piptaz Add vanc if - Septic - MRSA risk - Line-related infection
If shocked/need ICU, add gent
If colonisied with multiresistant bacteria, replace piptaz/gent with mero |
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Antiviral and antimould prophylaxis in haem malignancies |
High risk - acute leukaemia or MDS on chemo, GVHD - Posaconazole (anti-mould)
Low risk - intensive chemo for lymphoma, HSCT with expected neutropenia <14 days - Fluconazole
Everything else nil prophylaxis
Anti viral: for most haem maligs: valaciclovir or aciclovir |
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Ongoing febrile neutropenia at day 4-7 |
Consider pan CT including HRCT chest, sinuses Consider empiric antifungal - Amphotericin or voriconazole Aspergillus PCR if werent on antifungal prophylaxis |
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Antifungal mechanisms |
Azoles (fluconazole etc) - Inhibit synthesis of ergosterol (similar to cholesterol). Ergosterol is important for cell membrane structure and function Azole sterol
Polyene (Amphotericin) - Binds ergosterol, forming pores in cell membrane and ion leakage Lets the terrorists in (pores)
Echinocandin (Caspofungin) - Inhibit beta-glucan synthesis in cell wall synthesis (fungal equivalent of peptidoglycan) Casper floating atop the wall
Flucytasine - nucleic acid synthesis
Note ergosterol (azoles, amphoteracin) is membrane, beta glucan is wall |
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3 examples of moulds |
Aspergillus Mucor Scedosporium/lomentospora |
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Broadest antifungal |
Amphotericin Broadest antifungal Good tissue and cns penetrative |
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Invasive aspergillus diagnosis |
Gold standard is positive culture in a susceptible host plus either - Identification of fungal hyphae invading alveoli and blood vessels on histo - Isolation from a normally sterile site
But above is insensitive, so alternative is using scores, which mostly are based on have 1 of each: 1. Host risk factors 2. Clinical or radiological features (e.g. air crescent sign on HRCT) 3. Sputum/BAL culture/galactomannan or serum/BAL galactomannan/PCR |
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Aspergillus treatment |
Surgery when able Optimise host response (reduce immunosuppression, give GCSF etc)
Voriconazole or isavuconazole or amphoteracin Vori/isavuconazole is preferred to amph due to efficacy and tolerability 6-12 weeks then prophylaxis |
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Mucormycosis / zygomycosis Type of fungus 2 main sites Diagnosis Treatment |
Mould
Rhinocerebral in DIABETICS Pulmonary infection similar to aspergillus
Diagnosis is via culture only
Treatment Radical surgery Amphoteracin then posaconazole or isavuconazole |
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Scesosporium/lomentosporum 2 types and associated treatment |
Environmental opportunistic mould in immunocompromised people Can infect a range of organ systems
Treatment S. Apiospermum - sensitive to azoles, so voriconazole/posaconazole
L. Prolificans resistant to most antifungals, so surgery is mainstay |
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HIV proteins in viral entry |
HIV uses GP120 and GP41 to attach to CD4 and then to either CCR5 OR CXCR4 to gain entry CCR5 deletion can result in resistance (stem cell transplant with this has cured) |
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HIV infection timecourse |
HIV viral load goes up during first 3-4 weeks, then CD8 cells start killing CD4 cells, which cauzes cd4 count to go down and viral load to drop a little. Then causes viral illness Viral load then stabilises and goes slightly up over time as CD4 count slowly decreases Most viral infected cells dont produce the virus and so remain undected RNA transcriptase erroes keep occuring which result in new clones that overtime resulting in selection pressure towards ones that arent detected |
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Diagnosing HIV |
Previouslt western blot, now elisa Needs repeating at 6 weeks, 3 months, 6 months |
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Main HIV treatments |
Nucleoside RTIs (Stop RT from viral RNA to DNA) 'Ivir' or 'udine/abine' Tenofivir - nephrotoxic, osteoporosis Emtracitabine
Non-nucleoside RTI Irine or irdine Rashes HIV2 is resistant
Integrase inhibitors (Stop integration of viral DNA into human DNA) 'Tegravir' Dolutegravir: neural tube defects 0.3% rate
Protease inhitors 'Avir' (Stop cleavage of newly translated single viral protein unit into each individual protein) Exam question: ritonacir used to boost other antiviral effects
Test for HLAB something before giving abacavir due tk hypersensitivity |
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Initial HIB regimen |
2 NRTIs and either 1 NNRTI or 1 integrase inhibitor Sometimes a protease and 2 NRTIs |
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IE prophylaxis for non dental procedures |
Only if give if has a predisposing heart condition And Surgical prophylaxis would normally be given anyway. In which case, if it doesnt include coverage for the main IE organisms from that area, add extra coverage Eg gastro or GUT surgeries - main organism to worry about is enterococci, so add IV amoxycillin if not already covered |
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Peni ulcers 3 painful causes 2 painless causes |
Painful HSV Chancroid (haemophilus ducreyi) - Unilateral painful lymphadenopathy - Sharply defined, ragged borders Behcet
Painless Primary syphilis Lymphogranuloma venereum - Primary infection: painless ulcers, secondary 2-6 weeks after painful lymphadenopathy - Caused by chlamydia trachomatis - Treat with doxy |
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Features of legionella 1 history 3 lab 1 radiological 1 ECG |
Flu like illness with dry cough Hyponatraemia, lymphopenia, LFT derangement Pleural effusion (30%) Relative bradycardia |
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2 tapeworms |
Taenia Solium (cysticercosis/neurocysticercosis) - After food/drink contaminated by eggs - Neuro symptoms (seizure/headache) - CT: calcified lesions with no enhancement Echinococcus granulosus Both treated with bendazoles |
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Malaria What is it, and what cells does it reside in 2 most common types 2 types that cause recurrent disease Overall symptom Complicated (9 factors) vs uncomplicated disease Diagnosis Management Management of vivax and ovale |
Types Most common: falciparum & knowlesi Recurrent disease: vivax, ovale (due to dormant liver stage) Severe disease: falciparum then vivax What is it Parasitic amoeba - lives in RBCs Overall features
Febrile illness with an array of other variable features that don't differentiate it from other things (headache, cough, diarrhoea)
Diagnosis ?thick and thin films Micro or PCR (lowish sensitivity so repeat) Can be positive in people from an endemic area that have partial immunity without disease. Can also remain positive for some time after treatment
Complications - ARDS - Liver failure - Hypoglycaemia - AKI - Metabolic acidosis - Anaemia/haemolysis (Blackwater fever = haemolysis and AKI) - DIC / thrombocytopenia - Impaired consciousness/seizure - Parasite count >10%
Uncomplicated doesnt have any of the above, or parasite count >2% of red cells Complicated does
Management Uncomplicated - one of: - Oral artesunate + lemufantrine - Atovaquone + proguanol - Quinine and doxy or clinda
Complicated: - IV artesunate
- If above not available: IV quinine Vivax/ovale: - Add primaquine (to normal regimen) for 1-2 weeks, but test for G6PD function first as can cause haemolysis. And pregnancy |
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HIV and pregnancy ART for mother and baby Considerations for delivery Breastfeeding |
Avoid breastfeeding in all cases Continue ART during pregnancy Give baby ART prophylaxis for 4 weeks after delivery If inadequate viral load suppression at 36 weeks - Gice intrapartum zidovudine - Consider C section
Transmission is <2% with these measures |
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Toxins endo vs exo 3 examples of each |
Endotoxins (part of cell membrane) - all gram neg Shigella Lipopolysaccharide Vibrio cholerae - Increased cAMP, causing electrolye/fluid efflux Chlostridium tetani: lockjaw
Exotoxins (released) - mostly gram pos, some gram neg - Protein
Staph aureus - can cause diarrhoea Strep pyogenes Diphtheria - heart/liver necrosis |
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Measles 4 phases Multiple complications - most common - most common cause of death |
Phases 1. Incubation period 1-3 weeks 2. Prodrome 2-4 days - Fever, malaise - Then cough, conjuctivitis, coryza +/- koplik spots (white spots in mouth) 3. Exanthum - 2-4 days after fever - Starts in face and spreads down 4. Recovery - Cough may persist for 1-2 weeks - May have complication in this period (fever beyond 4 days after onset of rash suggests a complication Complications Most common otitis media Cause of death: pneumonia |
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Lyme diseae Cause 2 early features 2 later complications Investigation Management |
Spirochaete borrelia burgdorferi from tick bite Epidemiology America, Asia, Europe Not endemic to Australia - dont think there are any confirmed locally acquired cases But Australia is investigating into some other unknown ticborne chronic illness Clinical features Early - Erythema migrans - enlarging target rash at bite site (after 1 week) - Generalised stuff - headache, fever, lethargy, arthralgia
Late complications - Cardiac: heart block, myopericarditis - Neuro: facial nerve palsy, meningitis
Diagnosis Clinically by erythema migrans at tick site Confirm by elisa
Management Doxy if early Ceftriaxone if disseminated |
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2x viral meningitis associated with low csf glucose |
Mumps Herpes |
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Anthrax Organism Exposure Clinical feature Management |
Gram positive soil organism bacillus anthracis
90% cutaneous - black painless ulcer with surrounding oedema - from farm animals, especially south america, africa, asia, eastern europe Management cipro |
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Mnemonic for live vaccines |
Zac, you mustnt prescribe BCG incase they RIP Zoster (herpes, zaricella) Yellow fever MMR Polio (oral) BCG Influenza (intranasal only) Typhoid (oral) Rotavirus |
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Chlamydia symptoms (when symptomatic) Investigation Complication Management |
Women: discharge, bleeding Men: mucoid/watery discharge, dysuria
PCR - women vulvovaginal swab - men first catch urine
Complicatio PID
Mx: doxy, or azithro if likely to be non compliant |
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Bacterial vaginosis Cause, gram stain Results in what specific thing Clinical features Type of cells on micro Other positive test Treatment |
Bacterial overgrowth of vagina, most commonly by gardnarella vaginalis (gram + or - coccobacilli) Results in reduction in usual lactobacilli, causing increased pH
Offensive white discharge Not sexually transmitted, but commonly seen in sexually active people Micro: clue cells Positive whiff test
Management: metro |
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Giardia characteristic features Organism |
Watery, non-bloody diarrhoea (can be persistent) Long incubation period >7 days after exposure Flagellate protozoan Giardia Lablia |
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Approach to urethritis |
Take PCR for gonorrhoea, chlamydia and mycoplasma genitalium If purulent discharge (i.e. suspect gonorrhoea), take sample for culture (due to emerging gonococcal resistance) If purulent discharge, give ceftriaxone and azithro If non-purulent (i.e. not suspecting gonorrhoea), start doxy, or if suspecting non-compliance, single azithro |
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Bactericidal ABs Bacteristaric |
Penicillins, ceohalosporins Fluoroquinolones (cipro) Aminoglycosides Nitrofurantoin Metronidazole Bacteristatic Macrolides Tetracyclines Trimethorpim Sulphonamides Chloramphenicol |
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Aciclovir/ganciclovir mechanisms |
Guanasine analogue, inhibit DNA polymerase |
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Leprosy Cause Clinical features |
Mycobacterium leprae Patches of hypopigmented skin with sensory loss |
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4 vaccines contraindicated in all HIV |
Cholera Intranasal influenza Oral polio TB Dont give other live attenuated if cd4 less than 200 |
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5 Infectious causes of relative bradycardia |
Legionnaires disease Q fever Ricketsia Typhoid Psittacosis |
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Typhoid Clinical syndrome also known as Organism Acquired from/area Classical presentation Complications (3 organs) Features in FBC (3) Diagnosis Prevention Management |
Enteric fever Organism Salmonella typhi (a subspecies of salmonella enterica). The paratyphi subspecies cause a very similar illness Exposure
Contaminated food/water overseas (SE Asia, Southern Africa) Presentation
Classic presentation Late incubation: 5-21 days Week 1: lethargy with gradual, stepwise fever with relative bradycardia. May have headache, cough Week 2: abdo pain, rose spots (salmon coloured) Week 3: septic shock, intestinal perf, hepatosplenomegaly
Modern presentation less like above - suspect in any returned traveller with fever
FBC - Leukopenia, eosinopenia - Lymphocytosis
Complications - multi organs GI: intestinal haemorrhage, perforation Encephalitis Pneumonia
Diagnosis Stool and blood culture (BC positive in 50% of cases - gram neg bacilli) Management
Vaccination for prevention (but not that effective)
Cipro or azithro or ceftiaxone If from india, avoid cipro. If from pakistan, carbapenem (paki = penam) due to ESBL strains Severe disease: dexamethasone Assess for chronic carriage - if present give 4 weeks cipro |
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Chukungunya 2 uniqueish features |
Virus from mosquito Acute (3 weeks) Fever and severe arthralgia Post acute: 4-12 weeks, lethargy and ongoing arthralgia Chronic: ongoing synovitis |
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Histoplasmosis Organism Exposure factor Clinical features How it affects HIV |
Fungus Bird or bat droppings, esp bat caves or chicken houses 90% asymptomatic Otherwise pulmonary infection HIV at risk of disseminated disease |
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Shiga toxin producing E coli (STEC) 2 categories Which is the main E.coli that accounts for category 2 Clinical features (3) At risk of: Diagnosis Management |
Those that produce shiga toxin 2 (the bad one) aka high risk STEC, and those that dont (i.e. they just produce shiga toxin 1, which is less bad) E.coli o157:H7 makes up most of the shiga toxin 2 producers Diarrhoea that turns bloody by day 1-3 Abdo pain Often afebrile at presentation HUS days 5-13 Diagnosis: stoolt/rectal swab culture Management supportive. Dont givr antibiotics as these are associated with development of HUS |
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4 flaviviruses |
Dengue Japanese encephalitis Zika Yellow fever |
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Zika virus Type of virus 2 modes of transmission Clinical features (4-5) 2 complications Diagnosis Management |
Flavirus Mosquito, sexual for 3 months after disease Short incubation, median 5 days 4 to 7 day illness Pruritic rash (most) Myalgia, arthralgia Headache Conjunctivitis Fever in 50% Condoms for 3 months (6 months in outdated Australian guidelines) |
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Zika virus Type of virus 2 modes of transmission Clinical features (4-5) 2 complications Diagnosis Management |
Flavirus Mosquito, sexual for 3 months after disease
Short incubation, median 5 days 4 to 7 day illness Pruritic rash (most) Myalgia, arthralgia Headache Conjunctivitis Fever in 50%
Condoms for 3 months (6 months in outdated Australian guidelines) |
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Melioidosis |
Burkholdaria pseudomalei Gram neg rod (often blood cultured) Range of infections, commonly pneumonia Ceftazidime or mero for 10-14 days then 3-6 months of bactrim ?plus doxy Diabetes strongest risk factor |
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Hepatitis E Transmission 2 populations it can cause issues in |
RNA virus Usually asymptomatic, or self-limiting acute illness with elevated liver enzymes and then recovery South east asia, india, Africa, central America Pregnancy: 20% can get fatal fulminant hepatitis Immunocompromised, especially solid organ transplant recipients: can form a chronic hepatitis |
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Hepatitis E Transmission 2 populations it can cause issues in |
RNA virus Usually asymptomatic, or self-limiting acute illness with elevated liver enzymes and then recovery Long incubation period: 15-50 days
South east asia, india, Africa, central America Commonly pig meat
Pregnancy: 20% can get fatal fulminant hepatitis Immunocompromised, especially solid organ transplant recipients: can form a chronic hepatitis |
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R0 and how to calculate
Rt Herd immunity threshold Secondary attack rate |
R0Rate of news cases generated from a single case in afully susceptible population R0 = transmissibility X duration of infectiveness X rate ofcontact with other RtLike R0 except in a normal population rather than fullysusceptible population Herd immunity threshold1 – 1/R0 Secondary attack rateChance of a contacting the disease after contact with acase |
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Covid-19 structure and life cycle Type of nucleic acid What is the function of the spike protein |
Structure ssRNA (positive sense, meaning it can be used as mRNAstraight up) Spike protein- Binds to ACE2 to allow entry Life cycle 1. Spike protein binds to ACE2, allowing cell entry 2. Host proteases (TMPRSS2) allow uncoating 3. RNA used to translate proteins 4. RNA is replicated by RNA dependent RNA polymerase – target of remdesivir 5. New virions released |
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Covid Modes of transmission Infectivity - start date, main period of infectivity, end of infectivity |
Main one is direct transmission – droplet (<5microns,<1m travel) and contact Also airborne, but less so Incubation period median 6 days, range 2-21 People that never get symptoms can still transmit it Infectivity starts ~2 days before symptoms Most infectious on days 0-5 of symptoms (most likely to transmit on day of symptoms because haven’t started isolating) Infectious period ends (at ~day 10) before symptoms end |
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Covid-19 Investigations associated with poor prognosis |
High: - Ferritin - D dimer - Troponin - LDH - IL-6 Low: - Lymphocytes |
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Covid-19 management (need to update) |
DVT prophylaxis - With clexane. Possibly some evidence for intermediate doses
Corticosteroids - In all hospitalised patients on oxygen - Improved survival, especially ventilated patients
Tocalizumab - Hospitalised patients on oxygen - Improves mortality
Remdesevir - For hospitalised patients on low flow oxygen - Improved time to recovery, but no mortality benefit - Minimal benefit in high flow or NIV patients Convalescent plasma - not recommended - From donors of people with recovered COVID - Given to older people within 72 hours of symptom onset - Reduces progression to severe disease, but no mortality benefit MABs to spike protein, - In Straya: Casirivimab/imdevimab (spike protein MABs) - Not in straya: Bamlanivimib/etesevimab - Reduces recovery time when given within 10 days of symptom onset Non-hospitalised, no oxygen, risk factors for progression Inhaled budesonide - within 14 days of Sx onset Casirivimab/imdevimab - within 7 days Sotrovimab - within 5 days All patients on oxygen (including ventilated) - Dexamethasone - Casirivimab/imdevimab if seronegative - Tocalizumab/sarilumab (IL-6) or baracitinib (Jak 1+2) On oxygen, not ventilated - Remdesivir |
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Covid-19 associated invasive aspergillus |
Chronic steroid use is a risk factor |
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3 MRI findings in covid |
White matter lesions Basal ganglia lesions Strokes/ischaemic lesions |
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Antibiotic mechanism mastercard |
Protein synthesis 50s - Macrolides (azithro) - Linezolid 30s - Aminoglycosides (gentamicin) Beta-lactam/cell wall Folic acid synthesis - Trimethoprim |
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Post-exposure hepatitis B management needle stick 3 situations |
If person is immune (seroconversion after vaccine, or natural immunity from past infection, both of which I assume means a previous good hep B surface antibody titre) - Do nothing If source is hep b negative & contact if not immune, start hep B vaccination course If source is positive or unknown and contact is not immune: - Hep B immunoglobulin within 72 hours - Start immunisation course - Test surface antigen at baseline, 3 months and 6 months |
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Cholera toxin pathogenesis |
Secretory diarrhoea Triggers secretion of chloride out of the cell into the intestinal lumen via the CFTR Inhibits reabsorption via the NaCl channels Water follows |
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Tetanus wound management
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3 dose course, then booster every 10 years Do nothing if: - Hx of 3 dose course and booster in past years - Booster 5-10 years but clean wound Give booster if: - Anyone with Hx of <3 doses (also give Ig if wound dirty) - Hx 3 dose course, but booster >10 years - Hx 3 dose course, but booster >5 years ago and wound is dirty |
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4 vaccines for asplenic patients |
Haemophilus influenzae Pneumococcal Neisseria meningitidis Influenza |
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Malaria life cycle Which stage does primaquine act on? Artemesinin |
Mosquito injects sporozoites through the skin into the blood Enters liver, infects hepatocycte as a (schizont), where it rapidly divides Vivax and ovale have a dormant stage here as a hypnozoite (sleeping) Leaves liver as merozoite, and enters RBC and becomes trophozoite. Within the RBC they then mature to multi-nucleated schizonts. They then rupture, releasing gametocytes. Reinfects a new mosquito as a microgametocyte Within the new mosquito, somehow becomes a oocyst, that then releases sporozoites to then be reinjected back into a human Primaquine acts on hypnozoite stage in the liver Artemesinin acts on blood stage |
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