Infections (Chronic and Acute) Flashcards

1
Q

Type of parasite that causes malaria

A

Plasmodium

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2
Q

5 types of malaria

A

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

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3
Q

Most resistance malarial organism

A

Falciparum

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4
Q

Diagnosis of malaria

A

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

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5
Q

Uncomplicated vs complicated malaria features

A
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.

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6
Q

Treatment of uncomplicated malaria

A

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

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7
Q

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

A

primaquine is given as a one off

Can not give to G6PD def. patients - severe haemolysis

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8
Q

Which malarial parasites can lie dormant in the liver

A

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

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9
Q

Treatment of severe malaria

A

Artesunate IV or if unavailable then IV quinine

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10
Q

Additional therapy in severe malaria

A

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

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11
Q

HIV treatments regimen

A

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

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12
Q

Entry inhibitors

A

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

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13
Q

Nucleoside analogue reverse transcriptase inhibitors (NRTI)

A

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

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14
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTI)

A

examples: nevirapine, efavirenz

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

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15
Q

Protease inhibitors (PI)

A

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.

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16
Q

Integrase inhibitors

A

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

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17
Q

MOA azoles

A

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

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18
Q

Amphotericin B and nystatin MOA

A

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

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19
Q

Terbinafine MOA

A

Inhibits squalene epoxidase

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20
Q

Griseofulvin MOA

A

Interacts with microtubules to disrupt mitotic spindle

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21
Q

Flucytosine MOA

A

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

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22
Q

Caspofungin MOA

A

Inhibits synthesis of beta-glucan and major cell wall component

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23
Q

Name gram positive rods

A
Actinomyces
Bacillus anthracis (anthrax)
Clostridium
Diphtheria: Corynebacterium diphtheriae
Listeria monocytogenes
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24
Q

Gram positive cocci

A

Staph, Strep and enterococci

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25
Q

Gram negative coci

A

Neisseria and moraxella

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26
Q

Trimethoprim MOA

A

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)

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27
Q

Treponema pallidum diagnosis

A

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

28
Q

Tetanus

A

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

29
Q

MOA Vancomycin

A

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

30
Q

PCP pneumonia

A

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)

31
Q

Differentiate Legionella from mycoplasma pneumonia

A

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

32
Q

Jarisch-Herxheimer reaction

A

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

33
Q

Visceral leishmaniasis

A

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

34
Q

Hepatitis C

A

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

35
Q

Syphilis

A

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

36
Q

Live Vaccines

A
ROME I'm Your Big Travel Pest
Rubella, OPV, measles, epidemic typhus
Influenza
Mumps
Yellow fever 
BCG
Plague
Typhoid (active)
37
Q

Malignancies associated with EBV

A

Burkitt’s lymphoma
Hodgkin’s
Nasopharyngeal
HIV associated CNS

38
Q

Caspofungin MOA and family

A

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

39
Q

Azoles MOA

A

inhibit ergosterol synthesis

40
Q

Polyenes MOA

A

Bind ergosterol (Amphotericin and nystatin)

41
Q

Bugs fight back: Drugs affected by decreased permeability

A

Permiability barrier: trimethoprim, sulphonamide, vancomycin

Porin channels - beta lactams, aminoglycosides, chloramphenicol

42
Q

Bugs fight back: Inactivated enzymes

A

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

43
Q

Bugs fight back: Alteration of target site binding:

A

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

44
Q

Bugs fight back: Active efflux pump

A

Linezoild pumped out

45
Q

Bad prognsotic signs in Malaria Faciparum infection

A

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

46
Q

Bugs that commonly cause endocarditis

A

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

47
Q

First line therapy for native valve endocarditis.

A

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

48
Q

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

A

Flucloxacillin + Vancomycin + gentamycin

49
Q

Duration of Staph endocarditis therapy

A

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

50
Q

Duration of therapy for tricuspid valve endocarditis

A

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

51
Q

Strep endocarditis regimen

A

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

52
Q

HACEK group endocarditis

A

Ceftriaxone 2 g 4-6 weeks

53
Q

Causes of errythema Nodosum

A
NO cause found in 60%
Drugs (Sulfas)
Oral contraceptices
Sarcoid and lofgrens syndrome
Ulcerative colitis, Crohns and Bechet's 
Micro: Tb, Viral, Bacterial, Fungal
54
Q

Mantoux test: Cellular response

A

T cell response (delayed hypersensitivity)

55
Q

Interferon gamma release assay

A

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

56
Q

NAATs (Nucleic acid amplification test) For TB

A

Highly specific, relatively good 85% sensitivity)

Culture is the gold standard

57
Q

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

A

Get lots of fluid

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

58
Q

Treatment options for latent TB

A
9 months of Isoniazid: Hepatotoxic, 15% now resistant 
or
4 Months of Rifampicin 
or
3 months of rif and iso
59
Q

Standard short course TB treatment

A

2 Months of RICE and 4 months of Rif and Iso

60
Q

Hierachy of hepatitis in TB treatment

A

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

61
Q

Bedaquiline MOA

A

First novel agent - targets DNA synthase

62
Q

Delamanid MOA

A

Nitromidazole class that inhibits mycolic acid synthesis

63
Q

Treatment of MDR-TB

A

-Floxacin (Moxi or levo) + Bedaquiline + Linezolid

+ 2 second line drugs Clofazimine and Cycloserine

64
Q

How to treat TB in patients with HIV

A

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

65
Q

HIV meds to use in TB

A

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

66
Q

TB risk as per immunotherapy risk

A

Adalimumab > infliximab >etanercept