Infections Lecture 7: Guest Speaker: HIV Flashcards
What is the natural course of HIV virus
Acute infection: increase in amount of virus as you feel flu like symptoms called seroconversion illness (initial increase)
Immune system: helps reduce viral load for period of time, but replication is constant (evens out)
CD4 levels begin to drop as opportunistic infection occurs
Viral load increases as disease progresses
Describe what happens in the seroconversion stage of HIV
Person has HIV and develop antibodies to virus
High viral load and CD4 decline
Symptoms: Flu like
Not enough antibodies at this stage to test positive
Describe what happens in the asymptomatic stage of HIV
Immune system controls the HIV
CD4 count continues to decrease
Viral load continues to increase
Describe what happens in symptomatic stage of HIV and AIDS stage
Physical signs of HIV
Common cold Chest infection Skin problems Fever Weight loss
DEATH at AIDS stage
What sorts of infections are likely to affect you during AIDS
Mycobacterium tuberculosis
Pneumonia
Candidiasis
Herpes Simplex
What sort of malignancy is likely to affect you during AIDS
Lymphoma
Kapsi’s sarcoma
Cervical/anal cancer
How do you diagnose HIV
HIV immunoassay test for presence of HIV antibodies and p-24 antigen in blood
Then must have confirmatory test for HIV 1 and 2 differentiation assay
HIV nucleic acid test
How do you prevent HIV
Condom use
Testing and counselling
Use anti-retrovirals
PRE EXPOSURE PROPHYLAXIS
POST EXPOSURE PROPHYLAXIS
Needle exchange schemes
What are the aims of antiretroviral treatment
Achieve and maintain undetectable viral load
Strengthen immune system- increase CD-4 count
Reduce risk of opportunistic infection- if CD-4 count is less than 200 cells per micro litre
Reduce transmission risk
What is the mechanism of action of entry inhibitors CCR5 antagonist
Binding prevents the virus from entering immune cells via these receptors
What is the mechanism of action of Reverse transcriptase inhibitors (NRTI)
Inhibits enzyme responsible for viral RNA to DNA
Incorporates viral DNA chain leading to chain termination
Binds to active site on reverse transcriptase enzyme
What is the mechanism of action of Intergrase inhibitors
Bind to integrase enzymes, prevents integration of viral DNA to host DNA
What is the mechanism of action of protease inhibitors
Binds to active site of HIV-1 protease enzyme and prevents maturation of newly formed infectious virons
When should you start HIV treatment
When CD4 count is less than 350 cells per microlitre
If patient has hepatitis B or C co-infection, start at high CD4 count
Start in pregnancy regardless
What does the BHIVA treatment guidelines recommend you start with?
TRIPLE THERAPY
2 x NRTI treatment + third agent:
Example:
Truvada + Darunavir or ritonavir
Kivexa + efavirenz
What does Truvada treatment contain
Tenovir and emtricitabine
What does Kivexa treatment cotain
avacavir and lamivudine
What do you monitor for in a HIV patient
Well being
Side effects
Blood- liver, renal function, bone profile, lipids and glucose
Weight/BMI
Blood pressure
STI screen/sexual history
Hepatitis B or C marker
Surrogate markers- CD4 marker
What is the optimal CD4 count you should try to keep a patient with HIV at
200 or more cells per microlitre
What are the common side effects of anti-retroviral drugs
Headache Nausea, Vomiting Diarrhoea Rash RAISED LFTs
What are the specific side effects of Efavirenz, Atazanvir and tenofovir
Efvirenz- abnormal dreams, dizziness and drowsiness
Atazanavir- hyperbilirubinaema (yellowing of skin)
Tenofovir- renal impairment
What are the long term side effects of anti retroviral drugs
Fat redistributions- lipohypertrophy and lipoatrophy
Hyperlipidaemia
Hyperglycaemia
What is immune reconstitution syndrome
When antiretrovirals are started an overwhelming inflammatory response occurs as T cells that were once surpassed by HIV respond to previously acquired infection
May uncover opportunistic infections such as TB
Why do antiretrovirals have common interactions (hint: to do with how it is metabolised)
Protease inhibitors and NNRTIS are metabolised by cytochrome P450 isoenzyme CYP3A4 or CYP2D6
drug interaction Inducer: decreases drug level- failure of treatment
drug interaction Inhibitor: increases drug level- toxicity
