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Infectious disease, Oncology, & Urology > HIV-related illness, Hepatitis, TB > Flashcards

HIV-related illness, Hepatitis, TB Flashcards

1
Q

What is PCP? And how does it present?

A

Pneumocystis carinii pneumonia

An opportunistic FUNGAL infection

Non-productive cough, SOB, desaturating on exertion

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2
Q

What are the classic XR signs of PCP vs TB?

A

PCP: bilateral fine peri-hilar infiltrates

TB: apical cavitating lesions

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3
Q

What is CD4 count?

What is a normal range?

At what level are patients susceptible to what infections?

A

CD4 cells are T helper cells, which are directly attacked by the HIV

Normal range is 450 - 1600

Under 200 = susceptible to opportunistic infections like PCP, toxoplasmosis

Under 50 = susceptible to mycobacterium, CMV

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4
Q

What is AIDS?

One a patient has AIDS, they will always have it. True or false?

A

Presence of AIDS defining illnesses

Not based on CD4 count

False: a patient can present with AIDS, receive HAART and no longer have AIDS

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5
Q

List some AIDS defining illnesses?

A 
PCP
TB
Mycobacterium avium
Candidiasis
Cryptosporidosis
CMV
Herpes zoster
Salmonella
Toxoplasmosis

Kaposi sarcoma
Cervical cancer
Lymphoma (Burkitt’s)

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6
Q

What blood tests are useful to do for HIV?

When can they be relied upon?

A

Serological tests: only reliable 1 month post-exposure
Check if HIV+ve

CD4 count
Viral load
These assess how advanced the disease is.

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7
Q

Management of PCP?

A

Co-trimoxazole

Supportive

Also HIV treatment if they aren’t already on it - HAART

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8
Q

What is HAART?

What percentage compliance is needed for efficacy?

A

Highly active retroviral therapy

The use of 3 different anti-retroviral drugs which each act on the virus in a different way

95% compliance needed for efficacy

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9
Q

What prophylaxis is used to prevent which infections in HIV patients?

A

If CD4 count <200
- low dose co-trimoxazole for PCP and toxoplasmosis

If CD4 count <50
- azithromycin for TB

If recurrence of CMV: ganiciclovir

Latent TB should be treated, rifampicin and isoniazid

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10
Q

What types of HAART are there?

A

Nucleoside reverse transcrpitase inhibitors

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11
Q

How are all the Heps transmitted?

A

A: faecal oral, often shellfish

B: blood borne, sexual, vertical

C: blood borne, vertical, rarely sexual

D: blood borne (but only if B is present too)

E: faecal oral, often pork

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12
Q

Clinical features of all the Heps?

A 
Fevers
Jaundice
Nausea + vomiting
Abdo pain
Diarrhoea
Weakness, fatigue
Anorexia
Dark urine
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13
Q

Natural history of hep A?

Incubation, progression to chronic, immunity etc

A

Incubation is 2-3 weeks

Self-limiting infection

Only ever acute

100% immunity after

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14
Q

Natural history of hep B?

Incubation, progression to chronic, immunity etc

A

Incubation 1-6 months

Often self-limiting

Some cases lead to fulminant liver disease
Some cases lead to chronic Hep B

Chronic Hep B leads to cirrhosis and carcinoma

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15
Q

Natural history of hep C?

(Incubation, progression to chronic, immunity etc)

What proportion of Hep C cases lead to end-stage liver disease?

A

Following infection patients have mild illness they don’t seek help for.

Then infection becomes chronic

Some cases are severe, but these cases are more likely to clear the infection.

Once chronic, 1 in 3 chance of developing end-stage liver disease

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16
Q

What is fulminant liver disease?

A

Severe liver disease

17
Q

Natural history of hep D?

Incubation, progression to chronic, immunity etc

A

Needs Hep B antigens to survive so only found alongside Hep B

D is often the dominant infection

More risk of fibrosis if have B and D

18
Q

Natural history of hep E?

Incubation, progression to chronic, immunity etc

A

Usually self-limiting

Fulminant and chronic disease in immunosupressed

19
Q

Management of Hep A?

What about close contacts?

A

Supportive, monitor LFTs

Only a tiny % get severe liver failure

Post-exposure prophylaxis for contacts: vaccine and Hep A Ig

20
Q

Management of Hep B?

What about close contacts?

A

Supportive in acute infection, no treatment needed unless they plan to get pregnant soon.

Chronic:

  • pegylated interferon SC weekly for 48 weeks
  • oral tenofovir

You can’t cure Hep B, tx only reduces inflammation and controls viral replication

Post-exposure prophylaxis: vaccine and Hep B Ig

21
Q

Management of Hep C?

A

Pegylated interferon alpha SC weekly injection
PLUS
ribavirin PO
For 6 months

OR

Direct acting antiviral drugs

The aim is to cure

22
Q

Management of Hep D?

A

As with Hep B

  • pegylated interferon SC weekly for 48 weeks
  • oral tenofovir
23
Q

Management of Hep E?

A

Supportive

Monitor LFTs

24
Q

How is TB transmitted?

A

Droplet

Infectious patients cough up huge numbers of mycobacteria which can survive in the environment for ages.

25
Q

Describe what happens when someone first encounters TB?

A

Host macrophages engulf bacteria and carry them to hilar lymph nodes

Some organisms may disseminate to distant sites

Granulomas (tubercles) are formed to contain the bacteria

These can cause active TB immediately - primary TB

Or these may heal spontaneously and bacteria are eliminated

Or the are encapsulated but persist - latent TB

26
Q

What is miliary TB?

What is primary TB?

What is secondary TB?

A

Miliary: when primary infection is not adequately contained and invades the bloodstream

Primary: infection causing disease immediately

Secondary: a subsequent reactivation of latent TB, often precipitated by impaired immune system (HIV, malnutrition)

27
Q

Which patients are at risk of TB?

A

Close contact of a TB patient

Ethnic minority groups

Homeless, alcoholics, drug abusers

Poverty, malnutrition

Immunocompromised

Elderly patients
Children

28
Q

Clinical features of TB?

A 
Fatigue
Malaise
Fever, night sweats
Weight loss
Anorexia
Productive cough
Haemoptysis
SOB
Collapse
Effusion

Lymphadenopathy

29
Q

Investigations of TB?

A

Bedside:

  • obs
  • BM
  • ABG, VBG

Routine:

  • Bloods: FBC, UE, CRP, Clotting, LFTs
  • Cultures: blood, sputum
  • CXR

Specialist:

  • CT
  • MRI

Cultures:

  • Zeihl-Neelsenstain which shows if it’s an acid fast bacilli
  • Lowenstein-Jensen slope takes longer
  • sensitivies take a while
30
Q

What would you see on an XR in:

  • primary TB
  • secondary TB
  • miliary TB
A

Primary:

  • apical lesion
  • often LL lobe infiltrate
  • pleural effusion

Secondary:

  • no pleural effusion
  • apical lesions

Miliary:

  • millet seeds all over CXR
  • disseminated, widespread
31
Q

Where else can TB infect aside from the lungs?

A

GU:

  • kidney lesions
  • salpingitis
  • abscesses
  • epididymitis

MSK:

  • arthritis
  • osteomyelitis
  • nerve root compression

CNS:

  • meningitis
  • tuberculomas

GI:
- ileocaecal lesions

Lymph nodes: often hilar, paratracheal

Pericardial
- effusion

Skin

32
Q

Management of active TB?

A

Report to PHE

Isolation in a side room, protection for staff and visitors

Antibiotics:
6 months of R, I
First 2 months also give P and E

Supportive

Contact tracing

33
Q

What antibiotics are used in active TB treatment?

Give one side effect for each?

A

Rifampicin

  • orange urine
  • liver toxicity

Isoniazid

  • peripheral neuropathy
  • liver toxicity

Pyrazinamide
- liver toxicity

Ethambutol
- visual changes (loss of acuity, colour blindness)

34
Q

Management of latent TB?

Who should be treated?

A

Treatment should be considered if…

  • 35 yrs or younger
  • HIV
  • healthcare worker
  • strong mantoux response

Treatment is:

6 months of I
OR
3 months of R, I

35
Q

What supplement should you give alongside isoniazid? Why?

A

B6

Isoniazid can cause peripheral neuropathy

B6 helps prevent this

Infectious disease, Oncology, & Urology (11 decks)

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