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Infectious diseases > Uncommon infections > Flashcards

Uncommon infections Flashcards

TB, HIV

1
Q

AIDS associated lymphomas

A

Non-Hodjkins Lymphoma - DLBCL - Burkitts - Primary CNS lymphoma Hodjkins Lymphoma

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2
Q

What is Potts disease?

A

TB of the bone and spine. Most commonly lower thoracic and upper lumber vertebra cause kyphosis. Can also cause discitis and paravertebral and psoas abscesses.

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3
Q

What is the risk of TB reactivation?

A

Lifetime risk approx 10%. Increased risk if: HIV Immunosupression Genetic factors Smoking Vitamin D Diabetes and renal impairment Low body weight

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4
Q

What cells are important in the pathogenesis of TB?

A

Macrophages initially phagocytos the TB which they are then unable to destroy primarily due to blocking the binding of the phagosome with the lysosome. T cells are recruited by macrophages and cytokines eg TNFa and interferon. T cells then allow a formation of necrosis and granulomas

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5
Q

What is the incidence of TB in Australia?

A

5.7 per 100,000 86% of cases born in a endemic country

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6
Q

What is a Ghon complex?

A

A TB granuloma at the primary site (Ghon focus) and granulomas in the hilar lymph nodes.

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7
Q

What is the rate of extra-pulmonary TB and where can it occur?

A

Approx 20%, higher in HIV patients Lymph nodes Gastrointestinal Spine/bone - Potts disease CNS - meningitic, tuberuloma Pericardial Skin Genitourinary Miliary

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8
Q

Where does gastrointestinal TB most commonly present?

A

50% ileocaecal disease Can have mesenteric thickening or ascities TB peritonitis * 30% present as an acute abdomen

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9
Q

What are the poor prognostic factors for TB meningitis?

A

Advanced disease at diagnosis - focal neurology etc HIV Drug resistance

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10
Q

How is treatment different for TB meningitis?

A

Longer - 9-12 months Different drug - substitute ethambutol for moxifloxacin Add high dose dexamethasone then taper over 6-8 weeks Do not start antiretroviral treatment for at least 8 weeks

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11
Q

What is the mechanism of action and side effects of rifampicin?

A

RNA polymerase inhibition Hepatitis Thrombocytopenia Urine colour change to red/pink Multiple drug interactions GI upset

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12
Q

What is the mechanism of action and side effects of isoniazid?

A

Inhibits synthesis of myocoloic acid which is required for the cell wall. Hepatitis Rash/allergic reactions Polyneuropathy

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13
Q

What is the mechanism of action and side effects of pyrazinamide?

A

Unclear MOA, only works in acidic environment. Possibly inhibits fatty acid synthase 1. Hepatoxicity Skin rashes Joint pain and gout

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14
Q

What is the mechanism of action and side effects of Ethambutol?

A

It inhibits arabinosyl transferases which is required for cell wall biosynthesis. Only agent which is not hepatotoxic Arthralgia Optic neuritis which can cause colour blindness or decreased visual acuity

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15
Q

What are the risk factors for drug resistant TB?

A

Previous treatment CO-infection with TB and previous treatment Infection acquired in a high risk area Contact with known MDR-TB Failure to respond to initial treatment Exposure to multiple fluroquinolones

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16
Q

What is the treatment of TB?

A

2 months of: Isoniazide Rifampicin Pyrazinamide Ethambutol Then 4 months of: Isoniazide Rifampicin

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17
Q

When should hepatitis associated with TB treatment prompt cessation?

A

If >5x normal or >3x normal and symptomatic then either replace drugs if severe disease or pause treatment. Treatment can be restarted once levels <2x normal or close to baseline. Usually introduce one drug at a time

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18
Q

What is the most common drug resistance in TB? And what is its treatment?

A

Isoniazide 6RZE or 9R(z)E

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19
Q

What is the definition of MDR-TB?

A

Resistance to RIF and INH +/- other resistance

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20
Q

What is the definition of XDR-TB?

A

Resistance to RIF and INH and Quinolone and injectables (1 of amikacin, kenamycin or capreomycin)

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21
Q

Which TB drug has the most interactions with ART?

A

Rifampicin

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22
Q

What is the rate of HIV/TB co-infection?

A

3rd of HIV patients also have TB

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23
Q

For TB when is immune reconstitution inflammatory syndrome most dangerous?

A

TB meningitis

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24
Q

When should ART be started in TB/HIV co-infected patients?

A

If CD4<50 then start at 2 week post TB treatment If CD4>50 then can be started between 2 and 8 weeks If TB meningitis delay starting to at least 8 weeks despite CD4 count

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25
Q

What ART regimen is recommended while on TB treatment? Why?

A

Truvada (TDF + FTC) and double dose of raltegravir or dolvtegravir. Minimises interactions with rifampicin and alters dosing of those that do interact

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26
Q

What are the retroviruses which cause human disease?

A

Human T-cell Lymphotrophic virus 1 & 2 Human immunodeficiency virus 1 & 2

27
Q

What diseases are associated with HTLV 1?

A

Adult T-cell leukaemia/lymphoma Tropical spastic paraparesis or HTLV-1 associated myopathy

28
Q

What are the subtypes of HIV?

A

HIV 1 - M,N,O,P HIV 2 - A to H

29
Q

What are the co-receptors of HIV1?

A

CCR5 and CXCR4

30
Q

What are the CSF changes in TB meningitis?

A

Decreased glucose High protein Mononuclear pleocytosis Raised ADA

31
Q

What are the 3 stages of TB meningitis?

A

Prodromal non-specific illness Meningitic phase Paralytic phase

32
Q

What are the imaging findings of TB meningitis?

A

Basilar meningeal enhancement Hydrocephalus Cerebral oedema Infarcts

33
Q

How is HIV diagnosed?

A

Initial test for IgG antibody to the envelope. If this positive then confirm with Western blot or HIV viral load or antibody immunoassay.

34
Q

What is the use of testing for HIV viral p24 antigen?

A

Only detectable shortly after infection then disappears so not useful in the majority of cases

35
Q

What are the risk factors for PJP infection?

A

Any immunosupression notably: - HIV - Steroid used with other immunosuprresion - transplants - cell based immunosupresion - Haem cancers

36
Q

What is the treatment for HIV?

A

2x NRTI 1x other (INSTI, NNRTI, or PI with an enhancer)

37
Q

What are NRTIs? What are their mechanism of action?

A

These are a group of antiretrovirals Nucleoside and neucleotide reverse transcriptase inhibitors. Inhibit reverse transcriptase prevenitng DNA synthesis, act as DNA chain terminators. Abacavir Emtricitabine Lamivudine Zidovudine

38
Q

What are the NNRTIs? What are their mechanism of action?

A

Non-neucleoside reverse transcriptase inhibitors. Antiretrviral Inhibit HIV-1 reverse transcriptase by directly binding to the enzyme Tenofovir Efavirenz Etravirine Nevirapine Rilpivirine

39
Q

What are the common side effects of NRTIs?

A

Hepatotoxicity Lactic acidosis Metabolic syndrome

40
Q

What are the side effects of NNRTIs?

A

Rashes - mild to fatal Hepatotoxicity Multiorgan hypersensitivity

41
Q

What are the Protease inhibitors and what are their mechanism of action?

A

Antiretroviral Inhibit HIV aspartyl protease enzyme which is required for the production or viral proteins and enzymes Very large number, end in -navir

42
Q

What are the side effects and difficulties with protease inhibitors?

A
  • Alteration in lipid metabolism and BGL control - GI upset - Hepatotoxicity - Rash Need to be paired with a pharmacokinetic enhancer Extensive drug interactions
43
Q

What are the INSITs? What are their mechanism of action?

A

Antiretroviral Intergrase strand transfer inhibitors Inhibit HIV intergrase preventing viral DNA insertion into the human genome. Bictegravir Dolutegravir Eviegravir + cobicistat Raltegravir

44
Q

What is enfuvirtide? What are its main side effects?

A

An antiretroviral - fusion inhibitor It blocks gp41-mediated viral/cell fusion preventing infection. Subcut, used when other drugs fail SE - injection site reactions, bacterial pneumonia and hypersensitivity

45
Q

What is maraviroc?

A

An antiretroviral - CCR5 inhibitor Antagonist for the CCR5 receptor a co-receptor needed for viral fusion with the host cell. Only works in CCR5 tropic strains. SE - increased CVD, hypotension, hypersensitivity, immunosupression

46
Q

How is syphilis tested for?

A

Initial test is treponemal - EIA, TPPA, TPHA Then confirm with non-treponemal - RPR, VDRL

47
Q

What are the qualities of different syphilis tests?

A

Treponemal (EIA, TPPA, TPHA) are positive for life Non-treponemal (RPR and VDRL) are quantitative and falls after treatment. It can fall with time and be negative in tertiary syphilis

48
Q

What TB drugs are associated with hepatitis

A

Pyrazinamide > isoniazid > Rifampicin

49
Q

How can rifampicin resistance be tested?

A

By looking for the rpo6 gene via Xpert

50
Q

What is the treatment for Malaria?

A

Severe - IV artesunate or IV quinine Uncomplicated - PO artemether and lumefantrine If P Vivax or P Ovale then add primaquine for hepatic clearance

51
Q

Malaria subtypes

A

P Falciparum P Vivax P Ovale P Kowlesi P Malariae

52
Q

What are the causes of false negative mantoux tests?

A

Viral infection Sarcoidosis Malnutrition Hodgkin Lymphoma Immunosupression Overwhelming active TB

53
Q

What are the clinical features of dengue?

A
54
Q

What are the features of severe dengue?

A

Severe plasma leak

  • >20% haematocrit rise and matched drop after fluids

Severe haemorrhage

Organ impairment

55
Q

What is the pathogenesis of dengue?

A

Caused by flavivirus - RNA

4 serotypes which demonstrate antibody dependant enhancement

Transmisison via aedes mosquito (usually egypti)

56
Q

What is the incubation period of measles?

A

10-12 days

57
Q

What is the incubation period of dengue?

A

4 days

58
Q

What is the management of invasive aspergillosis?

A

Voriconazole

or

Amphotericin B (2nd line)

59
Q

What is the managment of cryptococcus meningitis?

A

Induction with amphotericin B + flucytosine then consolidation and erradication with fluconazole

Total treatment 12-18 months

60
Q

What is the diagnostic criteria for acute rheumatic heart disease?

A

Major:

  • Carditis
  • Subcutaneous nodules
  • Polyarthritis
  • Sydenems chorea
  • Erythema marginosum

Minor - PR interval prolongation, previous rheumatic fever, arthralgias, raised CRP, fever

2 major or 1 major and 2 minor

61
Q

What is the duration of penicillin prophylaxis for rheumatic heart disease?

A

10 years or until the age of 21 (whichever is longer)

For moderate disease til the age of 35

For severe disease or those requiring cardiac surgery til the age of 40 or lifelong

62
Q

What are the life cycle stages of malaria?

A
63
Q

What are the risk factors for IRIS?

A

CD4 <100

Cryptococcus or mycobacterial infection

Endemic areas of above infections

64
Q

How are genital ulcers differentiated?

A

Painful:

HSV

Chancroid

Painless:

Syphilis

LGV

Donovanosis

Infectious diseases (5 decks)

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