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Antiretroviral Therapy: Cheat Sheet by

CDC Stage of HIV Disease

-Stage I: Acute HIV infection
-Stage II: Asympt­omatic HIV
-Stage III: Early Sympto­matic HIV
-Stage IV: Late Sympto­matic HIV
= A Consti­tut­ional Disease
= B Neurol­ogical Disease
= C Secondary Infections
-C1 AIDS defining
-C2 Other infections
= D Secondary Cancers
= E Other Conditions

Clinical Staging of Oral Manife­sta­tions of HIV

Stage:
Adults and Adoles­cents (>15yo)
Children (<1­5yo):
1
No disease
No disease
2
Angular Chellitis, Recurrent oral ulcera­tions
Angular Chellitis, Linear gingival erythema, extensive warts, Recurrent oral ulcera­tions, Parotid enlarge
3
Persistent oral candid­iasis, Oral hairy leukop­lakia, Acute necrot­izing ulcerative stomat­itis, gingiv­itis, period­ontitis
Persistent oral candid­iasis (after 8wks), Oral hairy leukop­lakia, Acute necrot­izing ulcerative gingivitis or period­ont­itis.
4
Chronic (>1mo) orolabial HSV, Kaposi's sarcoma,
Chronic (>1mo) orolabial HSV, Karpo's Sarcoma, Non-Ho­dgkin's lymphoma

HIV-­related Oral Lesions:

Infect­ions:
- Fungal, Viral, Bacteria
Neoplams:
- Kaposi's Sarcoma, Non-Ho­dgkin's Lymphoma
Other:
- Aphtho­us-like Ulcers, Lichenoid or drug reactions, Salivary Gland Disease

Oral Candid­ias­is:

Erythe­matous Chelitis
Pseudo­mem­branous
Angular

Oral Ulcers:

-Herpes Simplex Infection
-HPV Lesiosn
-Cytom­ega­lovirus Infection
-Lymphoma
-Aphthous Ulcers
-Necro­tizing ulcerative gingiv­itis/ period­ontitis
-Histo­pla­smosis
-Necro­tizing Stomam­titis (NS)
There are many different causes of oral ulceration in patients with HIV infection = Herpes simplex infection, Varicella zoster infection. Accurate diagnosis and approp­riate management of oral ulceration in patients with HIV infection generally result in complete healing of the ulcera­tion.

Aphthous Lesions Clinical Types

Topical Therapy:
Intral­esi­onal:
Systemic Therapy:
Topical Cortic­ost­eroids
Triamc­ino­lone: 40 mg /ml (0.5 ml-1.0 ml injected bid)
Predni­sone: 0.5-1.0 mg/kg qd x 7-10d, then taper
   
Thalid­omide: 200 mg PO qd

Antire­tro­viral Cancer:

NRTIs:
Nucleoside OR Nucleotide Reverse Transc­riptase Inhibitors (Nukes)
NNRTIs:
Non-nu­cle­oside Reverse Transc­riptase Inhibitors (non-n­ukes)
PIs:
Protase Inhibitors
Fusion Inhibitors
Chemokine Receptor Antago­nists
Integrase Inhibitors
See Life cycle of HIV

Current Antire­tro­viral Targets

  

Reverse Transc­riptase Inhibi­tors:

Nucleoside Analogues Zidovudine (AZT, ZDV) Didanosine (ddI) Zalcit­abine (ddC) Stavudine (d4T) Lamivudine (3TC) Abacavir (ABC) Emtric­itabine (FTC)
Non-nu­cle­oside analogues: Nevirapine (NVP) delavi­rdine (DLV) Efavirenz (EFV) etravirine (ETV) rilpiv­irine (RPV)
Nucleotide analogue
Tenofovir (TFV)

Protease Inhibi­tors:

saquinavir (SQV)
ritonavir (RTV)
indinavir (IDV)
nelfinavir (NFV)
amprenavir (APV)
lopinavir (LPV)
fosamp­renavir (FPV)
atazanavir (ATV)
tipranavir (TPV)
darunavir (DRV)
dolute­gravir (DTG)

Reverse Transc­riptase Inhibi­tors:

Integrase Inhibitors
Fusion Inhibitor:
Entry Inhibi­tors:
ralteg­ravir (RAL)
fuzeon (T20)
maraviroc (MVC)
elvite­gravir (ELV)

NRTIs Mechanism of Action:

Nucleoside Analogs (like AZT):
Analog of thymidine, cytosine or guanine
 
Tripho­sph­ory­lated inside lympho­cytes to active compound.
 
Incorp­orate into growing HIV viral DNA strand by reverse transc­rip­tase.
Nucleotide Analogs:
tenofovir (TDF)
 
does NOT need to be tri-ph­osp­hor­ylated only di-pho­sph­ory­lated to activate compound.
After incorp­oration of NRTIs, viral DNA synthesis will be termin­ated.

Non-nu­cle­oside Reverse Transc­riptase Inhibi­tors:

Agents directly bind to reverse transc­riptase to inhibit transc­rip­tion.
NNRTIs do not require phosph­ory­lation to be active.

Protease Inhibitors (PIs) MOA:

Protease enzyme cleaves HIV precursor proteins into active proteins that are needed to assemble a new, mature HIV virus.
PIs bind to protease preventing the cleavage and inhibiting the assembly of new HIV viruses.

Fusion Inhibitor:

Chemokine Receptor Antago­nists:

Marviroc (Selze­ntry)
CCR5 or CXCR4 receptors on cell surface
Virus will bind to one of the 2 receptors (some pt virus will bind to either receptors)
Marviroc blocks viral entry at CCR5
Dosed 300mg BID= 150mg BID with P450 inhibi­tors. = 600mg BID with P450 inducers

Integrase Inhibitors

Ralteg­ravir (Isent­ress)
Dosed = 400mg BID (1tab BID)
No induction or inhibition on CYP450 enzymes or Pgp
Metabo­lized by UGT1A1 (glucu­ron­ida­tion) = Only affected by drugs that inhibit or induce UGTs (ie. rifampin)
 

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  • Published: 26th June, 2018

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