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RACP Written Exam 2015 > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

0
Q

What is the MOA of sulfonamides?

A

SulFOnamides eg Sulfamethoxazole inhibit FOlic acid synthesis

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1
Q

What is the MOA of macrolide antibiotics?

A

Macrolides (eg Erythromycin, Azithromycin, Clarithromycin, Roxithromycin) block protein synthesis by binding to the 50S ribosomal subunit

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2
Q

What is the MOA of Aminoglycosides?

A

Aminoglycosides (Gentamycin, Streptomycin) block protein synthesis by binding the 30S ribosomal subunit

(A”MINI”-glycoside = block the mini/smaller subunit)

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3
Q

What is the MOA of Quinolones / Fluoroquinolones?

A

(“People who wear FLUORO like to GYRATE in discoes”)

Inhibition of DNA gyrase / DNA topoisomerases

Fluoroquinolones - Cipro, Norflox, Moxifloxacin

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4
Q

How does Cutaneous Anthrax present?

A

Anthrax is caused by a gram positive rod, Bacillus anthracis.

It results in:
Black eschar
NO PUS
Painless with widespread oedema

Usually contracted by direct contact of bacteria into an open wound, usually by touching an infected animal.

Mortality is low with antibiotics, which contrasts with pulmonary anthrax.

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5
Q

In a E.Coli O157:H7 outbreak of diarrhoea, what measures would be most effective in reducing the transmission of this organism?

A

E.Coli O157:H7 is most commonly found in contaminated meat (Cattle are a major source).
Ensuring that meat products are thoroughly cooked will reduce transmission in an outbreak.
Raw meat should be separated from ready-to-eat food.
Hand wash AFTER handling raw meat.

Antibiotics are not routinely indicated.

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6
Q

How do you differentiate between tuberculous, viral and bacterial meningitis on CSF?

A

BACTERIAL:
glucose - low; LESS THAN HALF of plasma glucose
Protein - high >1.0g/L
White cells - 10-5000 polymorphs/mm3

VIRAL:
glucose - normal, or only mildly low (Always more than half of serum BSL)
Protein - high or normal
white cells - 15-1000 lymphocytes/mm3

TUBERCULOUS (similar to bacterial meningitis except a predominance of lymphocytes)
Glucose - low; LESS THAN HALF of plasma glucose
Protein - HIGH >1.0
White cells - 10-1000 lymphocytes/mm3

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7
Q

Hypervirulent strain C.Diff.

What is the mechanism of this strain of C.Diff?

A

Hypervirulent C.Diff aka “NAP-1/027 strain”
= an increased production of TOXINS A AND B (20x normal)

due to a mutation in a binary toxin (MUTATED TCDC GENE), whose normal action is to downregulate these toxins.

(TCDC = “The C. Diff Crazy” gene)
(C.Diff is a gram positive rod that forms spores)

Usually results from exposure to FLUOROQUINOLONES (15x rel risk) but also exposure to other Abx such as Cephalos, Macrolides)

The stool culture/C.Diff assay does not discriminate between the normal and Hypervirulent strain.

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8
Q

What are the clinical signs of severity in an episode of Hypervirulent C.Diff?

A 
NO further diarrhoea (due to Ileus)
Shock
High WCC
Low Albumin
renal impairment
Megacolon / Perforation / Ileus
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9
Q

What are the salvage regimens for C.Diff treatment (ie after trying Metronidazole and Vancomycin, and pulsed Vancomycin over a few weeks)

A

RIFAXIMIN and po Vancomycin

    • FIDAXOMICIN **
  • efficacy is as good as Vanc!
  • relapse rate is better than Vanc!
  • very expensive
  • works as a “macrocyclic antibiotic”, minimally absorbed

FAECAL TRANSPLANT

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10
Q

What are the common drug combinations used for treatment of HIV?
What are the side effects of these drugs?

A

Always Triple Therapy, including TWO Nucleoside Reverse Transcriptase Inhibitors (NRTIs)

  1. “TEE” - Tenofovir (NRTI) + Ermtracitabine (NRTI) + Efavirenz (NNRTI)
  2. “TER” - Tenofovir (NRTI) + Ermtracitabine (NRTI) + Ripilvirine (NNRTI)
  3. “TEA” - Tenofovir (NRTI) + Ermtracitabine (NRTI) + Atazanivir (PI) but also add Ritonavir (PI) to boost the effect of Atazanivir by saturating Cyp3a4

Side effects of:
TENOFOVIR - renal impairment
ERMTRACITABINE - minimal s/e!!
Efavirenz (NNRTI) - Psych/mood disorders / CNS disturbance
Protease Inhibitors (“-navir” drugs) - ** Increases CV risk **
Nevirapine - SJS!! Liver toxicity, Rash (“NEVER use NEViparine”)

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11
Q

A patient with newly-diagnosed HIV is found to have active TB. What is the next step in management?

A

DELAY antiretroviral therapy. Treat TB first.

Do not start antiretroviral therapy until 4-8 weeks after TB treatment to minimise Immune Reconstitution/IRIS.

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12
Q

What is the diagnosis & treatment for Cryptococcal Meningitis in HIV?

A

Symptoms- headache, fever, altered mental state.
Usually occurs when CD4 count is below 50.
DIAGNOSIS with CSF: Cryptococcal Ag positive, India Ink staining.

MANAGEMENT:

  • AMPHOTERICIN-B and FLUCYTOSINE for 2/52
  • followed by Fluconazole 8/52
  • then maintenance Fluconazole for 1 year until CD4 count is above 100 and sustained for at least 3 months

WATCH FOR IRIS –> may need Steroids.

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13
Q 
CD4 Countdown. 
What are the common AIDS-defining illnesses associated with these CD4 counts:
1. > 200
2. 100-200
3. 50-100
4. <50
A

CD4 counts:

  1. > 200
    - Oesophageal Candidiasis
    - TB (affects everyone- General population & HIV pts with high CD4 counts)
    - Kaposi’s Sarcoma
  2. 100-200
    - Pneumocystic Jiroveci (fungal. Rx Bactrim)
  3. 50-100
    - Respiratory Candidiasis
    - Toxoplasmosis Encephalitis (Rx ANTIFOLATE agents - Pyrimethamine-Sulfadiazine)
    - MAC, atypical mycobacterias (Rx Rifamp, Ethambutol, Clarithromycin)
  4. <50
    - CMV Retinitis / Enteritis / Pneumonitis (Rx Valganciclovir)
    - Cryptococcus Neoformans (fungal) meningitis
    - LYMPHOMAS
    - Progressive Multifocal Leukoencephalopathy
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14
Q

Features of Kaposi’s Sarcoma

A

Skin- purple nodules / Macules
Lymphoedema

Associated with Herpes Virus

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15
Q

What is Miraviroc?

A

CCR5 Receptor antagonist (Viral ENTRY Inhibitor)

Blocks signal 2 on CD4 T cells.

16
Q

Which antiretroviral drugs have good CNS penetration?

A

NRTIs - Abacavir (but increases CV risk!)
Zidovudine (S/E anaemia, neutropaenia, neuropathy)

NNRTIs - Nevirapine (S/E liver toxicity, rash, SJS)

PIs - Fosamprenavir-Ritonavir OR Idinavir-Ritonavir

17
Q

What happens to the GI lymphocytes in the first 2 weeks of HIV infection?

A

Early depletion of ALL LYMPHOCYTES / CD4 CELLS in the gut for the first 2 weeks of HIV infection

  • -> Leadpiped bowel for 2/52
  • -> Peyers patches and all lymphocytes lost
18
Q

Patient has HIV and neurocognitive issues.
What are the factors that increase risk of HIV-Associated Neurocognitive disorders?
What is the management?

A

Increased risk in:

  • Low CD4 count nadir
  • Hep C Co-infection (associated with neuroinflammation)

Symptoms range from mild to dementia.
Only 2% severe.

TREATMENT:
ABACAVIR (as long as no CV risk factors)

Or any of the antiretroviral drugs that cross the BBB that can lower the viral load in patient’s CSF (see other flash card)

19
Q

Define MDR TB and XDR TB.

A

MDR TB = resistance to Rifampicin and Isoniazid

XDR TB = resistance to Rifampicin, Isoniazid, FLUOROQUINOLONES AND AN INJECTABLE AGENT (Kanamycin / Amikacin (aminoglycoside) / Capreomycin)

20
Q

What is the standard short-course therapy for Tuberculosis?

A

2 months of RIPE, followed by 4 months of Rifampicin and Isoniazid.

Either a daily regimen or an intermittent regimen (3xweekly with DOT) can be used.

21
Q

What is the management for MDR TB?

A

Detect drug-resistance with “Rapid GeneXPert” tests for Rifampicin resistance.

Second-line drugs are necessary and the treatment duration is usually extended to 18-24 months.

DOT is recommended in all patients with drug-resistant TB to prevent further drug resistance.

Use RIPE
\+
MOXIFLOXACIN for 18 MONTHS
\+ 
INJECTABLE - AMIKACIN, KANAMYCIN (aminoglycosides)
22
Q

What is the management of TB in Pregnant women?

A

Pregnant women should be started on the STANDARD short-course therapy (RIPE)

When born–> Infants should be treated with Isoniazid.

Breastfeeding can continue.

23
Q

What is the management of TB in HIV patients?

A

Use STANDARD RIPE therapy (with DOT)
Plus Pyridoxine supplementation to decrease risk of peripheral neuropathy from Isoniazid.

** RIFAMPICIN IS ESSENTIAL (regimens without Rifampicin are less effective) but Rifampicin (Cyp inducer) interferes with antiretroviral agents!!! **

AVOID Saquinovir/RItonavir (PI) (contraindicated)
NEVer use NEVirapine (NNRTI) especially due to bad side effects - hepatotoxic, SJS.

Can continue to use TEE and TEA regimens.
TEN-ERM-Efavirenz (TEE) is best combination.

NEED TO DELAY ARV TREATMENT by 2 weeks if CD4 50 delay ARV by 4 weeks.

Watch for IRIS / paradoxical inflammatory response to TB treatment.

24
Q

What are the common side effects of TB drugs?

A

Isoniazid - PERIPHERAL NEUROPATHY, hepatitis
(Hence use Pyridoxine to prevent neuropathy in HIV pts)

Rifampicin (CYP 3A4 inducer) - interferes with HIV drugs –> increases HEPATOTOXICITY, GI upset, Pseudomembranous colitis

Ethambutol - OPTIC NEURITIS (need to check eyes during treatment), renal impairment

25
Q

What do you use for Pre-exposure prophylaxis in those at high risk of HIV infection?

A

TENOFOVIR- ERMTRACITABINE (TE-) dual therapy
Reduces risk by 45-75%

Use in MSM, IVDU, hetero with multiple partners in areas of high HIV prevalence, hetero-discordant couples (where one partner is HIV virus pos)

26
Q

Treatment for ESBL (multidrug resistant Gram negs)

A

CARBAPENEMS

or Ciprofloxacin

27
Q

Treatment of New Delhi Metallo-Betalactamase (MBL1)

A

COLISTIN
Or
TIGECYCLINE.

New Delhi MBL occurs in GRAM NEGs - E.Coli, Kleb usually

Produces a Carbapenemase –> hence RESISTANT to Carbapenems

RESISTANT to FQs and Aminoglycosides too.

28
Q

Treatment of VRE

A

Related to VAN gene - predominantly “VAN-B” VRE

USE LINEZOLID!!! Has good cover for Enterococcus faecalis AND faecium.

Enterococcus faecalis - sensitive to Amoxy/Ampi and (75%) Gent, AND LINEZOLID

Enterococcus faecium - sensitive to LINEZOLID.
Resistant to Amoxy/Ampi and only 50% sens to Gent

29
Q

What is the treatment of UNCOMPLICATED malaria caused by Plasmodium falciparum or P.Knowlesi (SE Asia/ mimics Falciparum)?

A

Treat patients IN HOSPITAL because a small proportion deteriorate after starting therapy.

(“Beyoncé KNOWLES discovers the ART of LOOM bands” = P.Knowles = ARTE-LUME)

** ARTEMETHER-LUMEFANTRINE combination (an Artemisinin-based combination) is the standard of care. **
(Total 6 doses - at 0, 8, 24, 36, 48 and 60 hours)
(Must be taken with fatty food or full-fat milk to aid absorption of Lumefantrine)

Chloroquine is NO LONGER USED as there is high-grade chloroquine-resistant Falciparum and Vivax in many parts of the world.

2nd line is Atovaquone-Proguanil, but DO NOT USE ATOVAQUONE-PROGUANIL IF IT WAS USED FOR PROPHYLAXIS.

There is emerging resistance to Artemesin in Thai/Cambodian border (due to mutation in propellor region of “Kelch” protein gene on Chromosome 13) but PROLONGED COURSE OF ARTEMESIN SEEMS EFFECTIVE.

30
Q

What is the treatment of P.Vivax and P.Ovale Malaria?

A

P.Vivax and P.Ovale can exist as DORMANT parasites (HYPNOZOITES) in the liver, which can reactivate disease.

** These patients need standard therapy (ART-LUME)
PLUS
PRIMAQUINE (14 days) to eliminate dormant parasites. **

** Primaquine can cause severe haemolysis in patients with G6PD deficiency hence need to exclude G6PD first. **

31
Q

What is the treatment for SEVERE Malaria?

A

SEVERE Malaria usually caused by P.falciparum. Features of severity:

  • altered consciousness
  • vomiting
  • jaundice
  • Renal imp/ oliguria
  • Resp distress
  • severe anaemia
  • acidosis
  • hypoglycaemia

THIS NEEDS URGENT IV ARTESUNATE

2nd line is IV Quinine but less effective than IV Artesunate.

Switch to oral treatment once clinically improved. Needs a full course (6 doses) of Art-Lume as for uncomplicated disease.

32
Q

What are the agents available for Malaria Chemoprophylaxis?

A

Atovaquone-Proguanil combo (with fatty food) daily dose.
Start 1-2 days prior, and continue for 7 days after malaria-prone area.

Or
Doxycycline - daily, continue for 4 weeks after malaria-prone area

Or
Mefloquine (Larium) - weekly, starting 2 weeks prior and continuing 4 weeks after malaria-prone area.

(ATOVAQUONE-PROGUANIL is the best agent as it is effective against the primary liver stages of malaria)
(Doxy and Mefloquine do not cover primary liver stages hence need to continue for 4/52 after returning home)

33
Q

Antibiotics with MRSA cover

A 
Vancomycin (glycopeptide)
Daptomycin
Linezolid 
Tigecycline
Ceftaroline
34
Q

Patient with HIV on ART, presenting with 6 months of bone pain, stress fractures and renal phosphate wasting. Which drug is the culprit?

A

Tenofovir.

Tenofovir is the HIV drug that is MOST associated with renal PO4 wasting –> Causes a Tenofovir-associated Fanconi syndrome.

PO4 gets better with stopping Tenofovir.

RACP Written Exam 2015 (14 decks)

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