Infections (Chronic and Acute)

Question 1

Type of parasite that causes malaria

Answer 1

Plasmodium

Question 2

5 types of malaria

Answer 2

P. Falciparum, P vivax, P knowlesi, P. Malariae and P. Ovale

Question 3

Most resistance malarial organism

Answer 3

Falciparum

Question 4

Diagnosis of malaria

Answer 4

Thick and thin films- however if antimalarials have been taken then this can mask the result.

Question 5

Uncomplicated vs complicated malaria features

Answer 5

Positive parasitology screen with Giemasa stain and thick and thin films. 
Severe malaria is defined as any of the following: 
parasite count higher than 2 % or 100, 000 per microlitre. 
Impaired consciousness
Jaundice
oliguria
Resp distress
Severe anaemia
Hypoglycaemia
Vomiting
clinical acidosis
AKI

In short- any end organ damage or signs of systemic illness.

Question 6

Treatment of uncomplicated malaria

Answer 6

Artemether + lumefantrine 10/120mg first line
atovaquone + proguanil 250/100 mg second line
Quinine + doxy 600/100 mg third line

Question 7

Which agent should be added in northern australia where human to host transmission is aiming to be limited

Answer 7

primaquine is given as a one off

Can not give to G6PD def. patients - severe haemolysis

Question 8

Which malarial parasites can lie dormant in the liver

Answer 8

Ovale and vivax: Hypnozoites are not eliminated by the uncomplicated malaria regimen. Primaquine or tafenoquine should be given.

Question 9

Treatment of severe malaria

Answer 9

Artesunate IV or if unavailable then IV quinine

Question 10

Additional therapy in severe malaria

Answer 10

Addition of ceftriaxone and paracetamol is recommended- especially if hypotensive.

Question 11

HIV treatments regimen

Answer 11

Typically made up of a nucleoside reverse transciptase inhibitor, Non-neucleoside transscriptase inhibitor and an integrase inhibitor

NRTI, NNRTI, Integrase inhib. Alternatively can have two NRTIs and an integrase

Question 12

Entry inhibitors

Answer 12

maraviroc (binds to CCR5, preventing an interaction with gp41), enfuvirtide (binds to gp41, also known as a ‘fusion inhibitor’)
prevent HIV-1 from entering and infecting immune cells

Question 13

Nucleoside analogue reverse transcriptase inhibitors (NRTI)

Answer 13

examples: zidovudine (AZT), abacavir, emtricitabine, didanosine, lamivudine, stavudine, zalcitabine, tenofovir
general NRTI side-effects: peripheral neuropathy
tenofovir: used in two recommended regime NRTI. Adverse effects include renal impairment and ostesoporosis
zidovudine: anaemia, myopathy, black nails
didanosine: pancreatitis

Question 14

Non-nucleoside reverse transcriptase inhibitors (NNRTI)

Answer 14

examples: nevirapine, efavirenz

side-effects: P450 enzyme interaction (nevirapine induces), rashes

Question 15

Protease inhibitors (PI)

Answer 15

examples: indinavir, nelfinavir, ritonavir, saquinavir
side-effects: diabetes, hyperlipidaemia, buffalo hump, central obesity, P450 enzyme inhibition
indinavir: renal stones, asymptomatic hyperbilirubinaemia
ritonavir: a potent inhibitor of the P450 system

It acts by inhibiting aspartyl protease enzymes, preventing viral maturation and prevents functional virion formation.

Question 16

Integrase inhibitors

Answer 16

block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell
examples: raltegravir, elvitegravir, dolutegravir

Question 17

MOA azoles

Answer 17

Inhibits 14 alpha demethylase which produces ergosterol (adverse) = P450 inhibition and liver toxicity

Question 18

Amphotericin B and nystatin MOA

Answer 18

Binds with ergosterol forming a transmembrane channel that leads to monovalent ion leak. Nephrotoxic

Question 19

Terbinafine MOA

Answer 19

Inhibits squalene epoxidase

Question 20

Griseofulvin MOA

Answer 20

Interacts with microtubules to disrupt mitotic spindle

Question 21

Flucytosine MOA

Answer 21

Converted to 5-Flurouracil, inhibitis thymidylate synthase and disrupts protein synthesis

Question 22

Caspofungin MOA

Answer 22

Inhibits synthesis of beta-glucan and major cell wall component

Question 23

Name gram positive rods

Answer 23

Actinomyces
Bacillus anthracis (anthrax)
Clostridium
Diphtheria: Corynebacterium diphtheriae
Listeria monocytogenes

Question 24

Gram positive cocci

Answer 24

Staph, Strep and enterococci

Question 25

Gram negative coci

Answer 25

Neisseria and moraxella

Question 26

Trimethoprim MOA

Answer 26

transient rise in creatinine: trimethoprim competitively inhibits the tubular secretion of creatinine resulting in a temporary increase which reverses upon stopping the drug trimethoprim blocks the ENaC channel in the distal nephron, causing a hyperkalaemic distal RTA (type 4). It also inhibits creatinine secretion, often leading to an increase in creatinine by around 40 points (but not necessarily causing AKI)

Question 27

Treponema pallidum diagnosis

Answer 27

Two main devisions: cardiolipin tests, trepnomal-specific anti-body tests. Examples of Cardiolipin tests are VDRL and RPR - these should become negative post treatment Treponemal specific antibody tests e.g. TPHA (Treponema pallidum haemagglutination tests) remains positive after treatment False positive cardiolipin tests in pregnancy, SLE, TB, leprosy, Malaria, HIV

Question 28

Tetanus

Answer 28

Exotocin from clostridium tetani (Gram +ve rod). Prevents relesae of GABA via tetanospasmin Supportive therapy is first line including benzodiazepines as a muscle relaxant. IM tentaus immunoglobulin can be administered in high risk individuals. Can give metronidazole

Question 29

MOA Vancomycin

Answer 29

inhibits cell wall formation by binding to D-Ala-D-Ala moieties, preventing polymerization of peptidoglycans Mechanism of resistance alteration to the terminal amino acid residues of the NAM/NAG-peptide subunits (normally D-alanyl-D-alanine) to which the antibiotic binds

Question 30

PCP pneumonia

Answer 30

PCP is the most common opportunistic infection in AIDS all patients with a CD4 count < 200/mm³ should receive PCP prophylaxis ``` Features dyspnoea dry cough fever very few chest signs ``` Management co-trimoxazole IV pentamidine in severe cases aerosolized pentamidine is an alternative treatment for Pneumocystis jiroveci pneumonia but is less effective with a risk of pneumothorax steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of respiratory failure by 50% and death by a third)

Question 31

Differentiate Legionella from mycoplasma pneumonia

Answer 31

Legionella: lymphopenia, hyponatraemia, dianosis on urinary antigen ``` Mycoplasma: Haemolytic anaemia or ITP Erythema multiforme GBS Myocarditic Seroligcal diagnosis ``` Both cause flu like illness, dry cough, and are treated with a macrolide

Question 32

Jarisch-Herxheimer reaction

Answer 32

fever, rash, tachycardia after the first dose of antibiotic in contrast to anaphylaxis, there is no wheeze or hypotension it is thought to be due to the release of endotoxins following bacterial death and typically occurs within a few hours of treatment No treatment is needed other than antipyretics if required

Question 33

Visceral leishmaniasis

Answer 33

By sand flys transmitting protozoa called leishman donovani - disease is AKA kala-azar Fevers, sweats, splenomegaly, weight loss, grey skin, pancytopenia Bone marrow or splenic aspirate

Question 34

Hepatitis C

Answer 34

RNA flavivirus Vertical tranmission rate 6% No vaccine 30% of patients will develop features: fatigue, arthralgia, fatigue HCV RNA is the investigation of choice for diagnosis Chronic hepatitis C: rheumatological problems (sjogren's syndrome), icrrhosis, HCC, cryoglobulinaemia (typically type II), membranoproliferative GN Interferon alpha and ribavirin: ribavirin is teratogenic

Question 35

Syphilis

Answer 35

G.Negative bacterium - obligate parasite - Spirochete Primary chancre is painless with a sloughy base and rolled boarder 3 stages: primary syphilis, secondary (6-12 weeks) - occurs with spirochetemia - non-itchy manulopapular rash - usually resolves in weeks to months, stage 3 is latent i.e. dormant, asymptomatic. Early phase within a year of infection Late phase after 1 year - which triggers tertiary syphilis: type 4 hypersens. reaction driven by T cells. Can cause aortitis from inflammation of vasa vasorum Neurosyphilis: Tabes dorsalis (wasting of dorsal column), can also get anterior spinal cord inflammation too ARGYLL ROBERTSON PUPIL: accommodates to a nearby object by loses light reflex Diagnosis: non-treponemal tests: RPR or VDRL and anti-cardiolipin antibody tests Trepenemal tests TPRA or FTA-ABS are specific to T pallidum

Question 36

Live Vaccines

Answer 36

``` ROME I'm Your Big Travel Pest Rubella, OPV, measles, epidemic typhus Influenza Mumps Yellow fever BCG Plague Typhoid (active) ```

Question 37

Malignancies associated with EBV

Answer 37

Burkitt's lymphoma Hodgkin's Nasopharyngeal HIV associated CNS

Question 38

Caspofungin MOA and family

Answer 38

Echinocandins, inhibits 1-3 B-D glucan synthesis . disrupts integrity of cell wall

Question 39

Azoles MOA

Answer 39

inhibit ergosterol synthesis

Question 40

Polyenes MOA

Answer 40

Bind ergosterol (Amphotericin and nystatin)

Question 41

Bugs fight back: Drugs affected by decreased permeability

Answer 41

Permiability barrier: trimethoprim, sulphonamide, vancomycin | Porin channels - beta lactams, aminoglycosides, chloramphenicol

Question 42

Bugs fight back: Inactivated enzymes

Answer 42

Beta lactamase, aminoglycoside modifying enzymes, esterases and acetyltransferase: Predominantly these organises are staph aureus, escappm organisms, E. COli, H. Influenza, N.Gonorrhoea, K pneumonia

Question 43

Bugs fight back: Alteration of target site binding:

Answer 43

Penicilin binding proteins made by MRSE, coag negative staph and strep pneumo. RIbosoms sites can alter streptomycin, erythromycin and tetracycline activity. DNA gyrase alteration for fluroquinolones RNA polymerase and DHFR - tetracyclines

Question 44

Bugs fight back: Active efflux pump

Answer 44

Linezoild pumped out

Question 45

Bad prognsotic signs in Malaria Faciparum infection

Answer 45

Schizonts on blood film, impaired consciousness, acidosis, Parasitaemia >10% or P.Knowlesi >0.5%

Question 46

Bugs that commonly cause endocarditis

Answer 46

Staph aureus, viridans strep, coagulase negative staph, enterococci, strep bovis and HACEK group of G negative bacilli Haemophilus, aggregatibacter, cardiobacterium hominus, eikenella corrodens, kingella

Question 47

First line therapy for native valve endocarditis.

Answer 47

Benzylpenicillin 1.8 g IV Q4H + Flucloxacillin 2 g Q4 H plus Gentamycin IV over 3-5 minutes (7mg/kg if otherwise well prior but needing ICU, 5mg/kg if not requiring ICU If MRSA is suspected e.g. people who inject drugs or higher risk groups then use vancomycin IV 30 mg/Kg IV loading If Penicillin allergic Cefazolin

Question 48

Therapy for infective endocarditis of foreign material e..g cardiac pacing wires, valves etc.

Answer 48

Flucloxacillin + Vancomycin + gentamycin

Question 49

Duration of Staph endocarditis therapy

Answer 49

4-6 weeks: if non-complicated 4 weeks, if complex like abscess or septic metastatic complications then 6 weeks

Question 50

Duration of therapy for tricuspid valve endocarditis

Answer 50

R sided MSSA endocarditis can have 2 weeks of fluclox IF No prostehetic, no metastatic infection e.g. OM, no cardiac complications, vege smaller than 20mm, clinical and micro response within 72-96 hours of therapy. Immunocompetent If MRSA or prosthetic valve - 6 weeks

Question 51

Strep endocarditis regimen

Answer 51

Ben pen and gent for 2 weeks if uncomplicated Single ben pen for 4 weeks can also be used Ceftriaxone for 2 weeks if allergic

Question 52

HACEK group endocarditis

Answer 52

Ceftriaxone 2 g 4-6 weeks

Question 53

Causes of errythema Nodosum

Answer 53

``` NO cause found in 60% Drugs (Sulfas) Oral contraceptices Sarcoid and lofgrens syndrome Ulcerative colitis, Crohns and Bechet's Micro: Tb, Viral, Bacterial, Fungal ```

Question 54

Mantoux test: Cellular response

Answer 54

T cell response (delayed hypersensitivity)

Question 55

Interferon gamma release assay

Answer 55

I.e. Quantiferon Gold Still may be negative in active disease. Doesn’t tell you latent or active Doesn’t tell you predictive value i.e. who will go one Detecting exposure to TB 4 tubes: CD4, CD8 as well as mitogen control and negative control looking at Interfron gamma background activity

Question 56

NAATs (Nucleic acid amplification test) For TB

Answer 56

Highly specific, relatively good 85% sensitivity) | Culture is the gold standard

Question 57

What is most important to do to increase dx yield on LP for TB meningitis ?

Answer 57

Get lots of fluid | In TB meningitis: Clinical suspicion and amount of fluid are important

Question 58

Treatment options for latent TB

Answer 58

``` 9 months of Isoniazid: Hepatotoxic, 15% now resistant or 4 Months of Rifampicin or 3 months of rif and iso ```

Question 59

Standard short course TB treatment

Answer 59

2 Months of RICE and 4 months of Rif and Iso

Question 60

Hierachy of hepatitis in TB treatment

Answer 60

P > I > R If 2-5 x ULN and asymptomatic then monitor If >5 or >3 with symptoms then stop Can give amikacin, ethambutol and moxifloxacin as liver sparing

Question 61

Bedaquiline MOA

Answer 61

First novel agent - targets DNA synthase

Question 62

Delamanid MOA

Answer 62

Nitromidazole class that inhibits mycolic acid synthesis

Question 63

Treatment of MDR-TB

Answer 63

-Floxacin (Moxi or levo) + Bedaquiline + Linezolid | + 2 second line drugs Clofazimine and Cycloserine

Question 64

How to treat TB in patients with HIV

Answer 64

CD4 <50 EARLY ART (before 2 weeks) - will increase IRIS risk but improve mortality >50 then ART by week 8 after starting TB therapy

Question 65

HIV meds to use in TB

Answer 65

Truvada (TDF + FTC (Emtracitabine)) + Raltegravir or dolutegravir

Question 66

TB risk as per immunotherapy risk

Answer 66

Adalimumab > infliximab >etanercept