HIV-related illness, Hepatitis, TB Flashcards
What is PCP? And how does it present?
Pneumocystis carinii pneumonia
An opportunistic FUNGAL infection
Non-productive cough, SOB, desaturating on exertion
What are the classic XR signs of PCP vs TB?
PCP: bilateral fine peri-hilar infiltrates
TB: apical cavitating lesions
What is CD4 count?
What is a normal range?
At what level are patients susceptible to what infections?
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
What is AIDS?
One a patient has AIDS, they will always have it. True or false?
Presence of AIDS defining illnesses
Not based on CD4 count
False: a patient can present with AIDS, receive HAART and no longer have AIDS
List some AIDS defining illnesses?
PCP TB Mycobacterium avium Candidiasis Cryptosporidosis CMV Herpes zoster Salmonella Toxoplasmosis
Kaposi sarcoma
Cervical cancer
Lymphoma (Burkitt’s)
What blood tests are useful to do for HIV?
When can they be relied upon?
Serological tests: only reliable 1 month post-exposure
Check if HIV+ve
CD4 count
Viral load
These assess how advanced the disease is.
Management of PCP?
Co-trimoxazole
Supportive
Also HIV treatment if they aren’t already on it - HAART
What is HAART?
What percentage compliance is needed for efficacy?
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
What prophylaxis is used to prevent which infections in HIV patients?
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
What types of HAART are there?
Nucleoside reverse transcrpitase inhibitors
How are all the Heps transmitted?
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
Clinical features of all the Heps?
Fevers Jaundice Nausea + vomiting Abdo pain Diarrhoea Weakness, fatigue Anorexia Dark urine
Natural history of hep A?
Incubation, progression to chronic, immunity etc
Incubation is 2-3 weeks
Self-limiting infection
Only ever acute
100% immunity after
Natural history of hep B?
Incubation, progression to chronic, immunity etc
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
Natural history of hep C?
(Incubation, progression to chronic, immunity etc)
What proportion of Hep C cases lead to end-stage liver disease?
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
What is fulminant liver disease?
Severe liver disease
Natural history of hep D?
Incubation, progression to chronic, immunity etc
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
Natural history of hep E?
Incubation, progression to chronic, immunity etc
Usually self-limiting
Fulminant and chronic disease in immunosupressed
Management of Hep A?
What about close contacts?
Supportive, monitor LFTs
Only a tiny % get severe liver failure
Post-exposure prophylaxis for contacts: vaccine and Hep A Ig
Management of Hep B?
What about close contacts?
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
Management of Hep C?
Pegylated interferon alpha SC weekly injection
PLUS
ribavirin PO
For 6 months
OR
Direct acting antiviral drugs
The aim is to cure
Management of Hep D?
As with Hep B
- pegylated interferon SC weekly for 48 weeks
- oral tenofovir
Management of Hep E?
Supportive
Monitor LFTs
How is TB transmitted?
Droplet
Infectious patients cough up huge numbers of mycobacteria which can survive in the environment for ages.
Describe what happens when someone first encounters TB?
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
What is miliary TB?
What is primary TB?
What is secondary TB?
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)
Which patients are at risk of TB?
Close contact of a TB patient
Ethnic minority groups
Homeless, alcoholics, drug abusers
Poverty, malnutrition
Immunocompromised
Elderly patients
Children
Clinical features of TB?
Fatigue Malaise Fever, night sweats Weight loss Anorexia
Productive cough Haemoptysis SOB Collapse Effusion
Lymphadenopathy
Investigations of TB?
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
What would you see on an XR in:
- primary TB
- secondary TB
- miliary TB
Primary:
- apical lesion
- often LL lobe infiltrate
- pleural effusion
Secondary:
- no pleural effusion
- apical lesions
Miliary:
- millet seeds all over CXR
- disseminated, widespread
Where else can TB infect aside from the lungs?
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
Management of active TB?
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
What antibiotics are used in active TB treatment?
Give one side effect for each?
Rifampicin
- orange urine
- liver toxicity
Isoniazid
- peripheral neuropathy
- liver toxicity
Pyrazinamide
- liver toxicity
Ethambutol
- visual changes (loss of acuity, colour blindness)
Management of latent TB?
Who should be treated?
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
What supplement should you give alongside isoniazid? Why?
B6
Isoniazid can cause peripheral neuropathy
B6 helps prevent this
