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Aids approach patients

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AIDS

AIDS

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  • TQ... sir... I hope we can spread our knowledge,,,,
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  • Several antiretroviral drugs are both CYP 450 & P-gp substrates, it is therefore not uncommon to encounter interactions among them or with agents used to treat other conditions. NRTIs: are eliminated renally and are not substrates for the CYP 450 enzymes or drug transport proteins and thus not prone to the most common pharmacokinetic drug interactions. Integrase inhibitors are also not metabolised via CYP450, raltegravir undergoes glucoronidation and is less susceptible to drug interactions. Most of the drug interactions known to affect UGT, non are known to affect raltegravir’s efficacy and no dosage adjustments have been recommended.The NNRTIs, PIs, and CCR5 inhibitors are all substrates of CYP450 and most available drugs are substrates of CYP4503A making them prone to a number of drug interactions.
  • Transcript

    • 1. STAND
      UNDER
      ACQUIRED
      DEFICIENCY
      IMMUNO
      SYNDROME
    • 2.
    • 3. WE NEED TO KILL THEM
    • 4. BEFORE THEY KILL US?
    • 5. SO
      WE
      MUST
      KEEP TRYING
    • 6. …AND KEEP TRYING
    • 7. UNTIL
      THE END
    • 8. "You Cannot Teach Old Dogs New Tricks"
      Prof Adeeba
    • 9. Normal
      Immune
      System
      …will protects the body
    • 10. It consists of
      LYMPHOID
      organs and
      tissues
      ..which kills
      bad organism
    • 11. HIV will attack
      THE SYSTEM
      AIDS
      and it becomes
    • 12. AIDS
      COMES FROM
    • 13.
    • 14. also from…
    • 15. blood transfusion
    • 16. to
      Mother
      baby
    • 17. IF U
      HAVE THESE
    • 18. ORAL CANDIDIASIS
    • 19. Oral Hairy
      Leukoplakia
    • 20. …or these…
    • 21.
    • 22. Acquired Immunodeficiency Syndrome (AIDS)
      Acquired Immunodeficiency Syndrome (AIDS) is caused by a retrovirus known as the Human immunodeficiency Virus (HIV).
    • 23. Acquired Immunodeficiency Syndrome (AIDS) - definition
      Is a conglomerate of signs and symptoms arising from the development of opportunistic infections and unusual tumours which arise as a result of a failing immune system.
      Clinical definition of AIDS consist:
    • 24. AIDS defining diagnosis
    • 25. Immunology and Natural History of HIV/AIDS
    • 26. The Normal lmmune System
    • 27. Human Immunodeficiency Virus
      HIV is a retrovirus. (RNA)
      Uses host’s DNA (lymphocytes) to make viral DNA and to replicate itself.
      Host lymphocytes infected with HIV have a very short lifespan.
      HIV continuously uses new lymphocyte to replicate itself.
      Up to 10 million individual viruses are produced daily.
      • Causing severe damage to and eventually destroys the immune system.
    • 28.
    • 29. HIV Co-receptors
    • 30. Viral variation in HIV infection
    • 31. The effect of HIV on the immune system is monitored by measuring the CD4 lymphocyte count in the blood.
      A normal CD4 count 600 and 1,200 cells/µ.
      CD4 counts <350 cells/µL indicate that some impairment of immune function.
      CD4 counts <200 cells/µL - risk of serious opportunistic infections
    • 32. HIV: Two Types Recognized
    • 33. Epidemiology
    • 34. AIDS - Classification
    • 35. Modes of Transmission
    • 36. CLINICAL MANIFESTATION of HIV
      MOHD HANAFI RAMLEE
    • 37.
    • 38. Incubation
      2 - 4 weeks after exposure but may be as long as 6 weeks.
      Symptoms tend to develop abruptly and last for 1.5 - 2 weeks.
    • 39.
    • 40. Acute Sero-conversion Phase or Primary HIV-1 infection
      60-90%
      difficult to identify (not remember the flu-like illness, common cold).
      This glandular fever  2 to 6 weeks after exposure.
      However this mononucleosis-like illness  prolonged and may last 2-4 weeks.
      acute encephalitis-like illness with reversible encephalopathy
      disorientation,
      impairment of consciousness
      cognitive functions
      Recovery is complete and the patient will feel well.
      Occasionally the acute seroconversionillness may be completely asymptomatic.
    • 41. Asymptomatic HIV infection
      early stages
      progressive fall of CD4+ T-lymphoeyte
      symptoms and signs will become apparent.
      2 to 7 years before the appearance of constitutional symptoms which may herald the onset of AIDS.
    • 42. Persistent Generalised Lymphadenopathy (PGL) - Symptoms
      CD4+ T-lymphocytes progressively decline
      The commonest not specific symptoms and signs encountered in the early stages are:
      · Malaise
      · Lethargy
      · Loss of appetite
      · Loss of weight
      · Diarrhoea
      · Intermittent fever
    • 43. Persistent Generalised Lymphadenopathy (PGL) - Signs
      weight loss of more the 10% the ideal body weight,
      prolonged fevers of more than 3 months,
      Persistent generalised Iymphadenopathy of more than two groups of Iymph nodes.
      multi-dermatomalherpes zoster,
      oral candidiasis
      oral hairy leukoplakia
    • 44. Herpes Zoster
      Herpetic lesions in HIV-infected patients are caused by reactivation of the latent virus. Although mucocutaneous lesions may appear in any region of the body, the most common sites are the genital, perianal area.
    • 45. Oral Candidiasis
      Oral candidiasis "thrush" is an infection of yeast fungi of the genus Candida on the mucous membranes of the mouth. It is frequently caused by Candida albicans, or less commonly by Candida glabrata or Candida tropicalis.
      Oral Hairy Leukoplakia
      Hairy leukoplakia is seen in severe defects of immunity, particularly in HIV infection. The cause of this condition is an opportunistic infection by the Epstein-Barr virus (EBV). After the primary EBV infection has been overcome, the virus stays latent in the B cells and also causes lytic infection in the oropharynx, controlled by the immune system. Uncontrolled lytic infection in the oropharynx is manifested as oral hairy leukoplakia in immunosuppressed hosts. Oral hairy leukoplakia is not associated with any malignant potential.
    • 46. Persistent Generalised Lymphadenopathy (PGL) - Labs
      Lymphopenia
      Leukopenia
      Thrombocytopenia
      Anaemia
      Reduced CD4+ T-lymphocyte count
      Decrease ratio of CD4+/CD8+
      Raised gamma-globulins
      Cutaneous Anergy
    • 47. Persistent Generalised Lymphadenopathy (PGL) - Markers
      Absolute platelet counts
      Total Lymphocyte count
      CD4+ T-lymphocyte count (cells/uL)
      CD4+/CD8+ Ratio
      p24 antigen
      beta 2-microglobulins
      Serum Neopterin
      PCR-RNA-HIV
    • 48. AIDS
      10% of patients develop an AIDS-defining illness with a CD4 count above 200 cells/mm3.
      The median time to development of an AIDS defining illness is 12 – 18 months (if not on opportunistic infection prophylaxis or antiretroviral therapy).
      Median CD4 count at the time of developing an AIDS-defining illness is 67 cells/mm3.
      Median survival after CD4 count falls below 200 cells/mm3 is 38 – 40 months.
    • 49. AIDS
      Consist of
      Pulmonary TB, Recurrent pneumonia, Invasive Cervical Cancer
      CD4+ T-lymphocyte counts
      declining immunity
      opportunistic infections
      atypical tumours.
    • 50. Advance AIDS (CD4 < 50)
      Median survival is 12 – 18 months (if not on opportunistic infection prophylaxis or antiretroviral therapy).
      Cytomegalovirus disease and disseminated Mycobacterium avium complex tend to occur at this stage.
    • 51. Factors affecting rate of progression
      Acute HIV syndrome:
      Prolonged presence of symptoms correlates with a more rapid progression of disease.
      Strong HIV-specific CD8 cytotoxic T cell and CD4 T cell responses correlate with a slower progression of CD4 cell decline.
      Co-infections
      Hepatitis
      Cytomegalovirus
      Mode of transmission
      Blood transfusion recipients progress more rapidly than patients who acquire it sexually or by injection drug use.
    • 52. Factors affecting rate of progression
      Age.
      Older patients progress faster than younger patients.  
      Viral load.
      Patients with higher viral loads will progress more rapidly.
      Genetic modifiers.
      Strain variations.
    • 53. Factors affecting rate of progression
      Effect of prophylaxis of opportunistic infections on the course of HIV disease
      PCP
      Disseminated MAC
      Experience of the medical provider
    • 54. Factors affecting rate of progression
      Effect of antiretroviral therapy on the course of HIV disease.
      3-drug therapy (HAART) >> 2-drug therapy > Monotherapy
      When therapy is started in the early asymptomatic infection period the estimated mean time to development of AIDS is 8 months for patients treated with monotherapy, 9.8 years with double therapy and 20 years with HAART
    • 55. Kaposi’s Sarcoma
      tumour of the blood vessel.
      Classical:
      elderly males of Mediterranean descent.
      confined to the lower limbs.
      previously healthy young males will suggest the presence of concomitant HIV
      numerous and fairly extensive.
      confined to the skin, lungs with hemorrhagicpleural effusion.
    • 56. Kaposi Sarcoma
      With the rise of the AIDS epidemic, KS, as initially one of the most common AIDS symptoms, was researched more intensively in hopes that it might reveal the cause of AIDS. The disease was erroneously referred to as the "AIDS rash".
    • 57. Natural History:
    • 58. Clinical Features
    • 59. Acute Retroviral Rash
      5-10 mm macular or papular erythematous lesions usually on face and trunk but may involve extremities.
      Rash usually starts 48-72 hours after the fever starts and may last for 5 – 8 days.
      It may be slightly pruritic but usually is not.
      Oral, esophageal, anal or genital ulcerations are painful, shallow and well demarcated.
    • 60.
    • 61. Opportunistic Infection
    • 62. CD4 count and OIs
      TB
      PCP, thrush
      Toxo, Esoph thrush
      Below 200
      PML
    • 63. HIV-Related Complications
    • 64. Pneumocystis Carinii (PCP)
      Pneumonia with hypoxemia
      Insidious
      CXR with bilateral disease but can vary
      High morbidity and mortality
      CD4 generally below 200 or < 14%
      Significant alveolar disease (elevated LDH)
      Silver stain of sputum or BAL for diagnosis
    • 65. PCP - Interstitial Infiltrates
    • 66. Treatment of PCP
      Determine level of hypoxemia and need for hospitalization
      TMP-SMX is the most efficacious treatment
      Alternatives exist in those allergic to sulfa
      Steroids indicated if pO2 < 70
      May get worse before improvement seen
      Usually need to R/O other pathogens
    • 67. Prevention of PCP
      Oral TMP-SMX is prophylaxis of choice
      Alternatives exist (dapsone, pentamidine, etc)
      10 prophylaxis: CD4 < 200
      20 prophylaxis with history of prior PCP
      Still being determined is whether prophylaxis can be withdrawn after beneficial effects of HAART
    • 68. CNS Toxo vs CNS Lymphoma
    • 69. Toxoplasmosis
    • 70. Treatment / Prevention of Toxo
      Rx: Sulfadiazine + Pyrimeth. + Folinic Acid
      Sulfa allergic: Clinda + Pyrimeth. + Folinic A.
      Repeat MRI to make sure lesions smaller
      Maintenance therapy after induction
      Consider steroids and anticonvulsants
      TMP-SMX is adequate 10 prophylaxis
      dapsone and pentamidine is not protective
      should protect when CD4 < 100 if IgG +
    • 71. Cryptococcal Meningitis
      Very subtle presentation at times
      HA, fever, lethargy, nausea
      Imaging studies usually normal
      CSF generally with high opening pressure, mild lymphocytic pleocytosis
      CSF with + India Ink, crypto Ag, yeast
      Serum crypto Ag can screen HIV cohorts
    • 72. Cryptococcus - India Ink Stain
    • 73. Treatment of Crypto Meningitis
      Most induce with ampho B +/- 5FC
      Can also use high dose fluconazole if unable to tolerate Ampho B
      Will need chronic maintenance to control infection as cannot be generally cured
      High risk for recurrent elevated ICP which can result in hydrocephalous
      May require periodic removal of CSF
    • 74. CMV Retinitis
      Results in floaters and decreased vision
      Seen in those with CD4 < 50-100
      Diagnosis by ophthalmologic exam
      It is a disseminating infection
      Difficult systemic treatment with an induction and maintenance treatment
      gancyclovir, foscarnet, cidofovir
    • 75. Mycobacterium Avium Complex
      Not uncommon when CD4 < 75
      Chronic constitutional symptoms such as fever, sweats, and weight loss
      Labs may reveal anemia, leukopenia,and elevated alk phos
      CT of abdomen may see periaortic or retroperitoneal adenopathy and HSM with a relative paucity of peripheral adenopathy
    • 76. MAC Diagnosis and Treatment
      AFB BC has high yield but takes weeks
      Bone marrow staining and culture
      Treatment requires a minimum of 2 meds chronically as it is quite resistant
      macrolide, ethambutol (amikacin, rifabutin, cipro)
      10 Prophylaxis with macrolide in those with CD4 <75
    • 77. Oropharyngeal Infections
      Candidiasis
      Oral Hairy Leukoplakia (OHL)
      Ulcer Disease
      Periodontal Disease
      Kaposi’s Sarcoma
    • 78. Oral Candidiasis
      >60% of patients with CD4 <100 cells/mm3
      Often Asymptomatic or altered taste, burning, odynophagia
      Four Forms
      Pseudomembranous
      Erythematous
      Angular Cheilitis
      Hyperkeratotic
    • 79. Pseudomembranous Oral Candidiasis
      White patches that can be scraped off leaving erythematous base
    • 80. Erythematous Oral Candidiasis
      Smooth red patches, found on tongue and cheeks
    • 81. Angular Cheilitis
      Cracking and fissures at corner of mouth
    • 82. Hyperkeratotic Oral Candidiasis
      Thickened white patches, do not scrape off
    • 83. Oral Candidiasis: Diagnosis
      Diagnosis is often clinical, based on typical appearance
      KOH preparation of scraping for hyphae, pseudohyphae, and budding yeast
      Helpful especially for erythematous and hyperkeratotic disease
    • 84. Oral Candidiasis: Treatment
      Initial topical therapy
      Clotrimazole troches 10mg 5x/day
      Nystatin swish & swallow 500,000 units QID
      Refractory to topical treatment
      Fluconazole 100 mg QD
      Itraconazole 100 mg BID
    • 85. Oral Candidiasis: Treatment
      Fluconazole Refractory Disease
      Higher dose fluconazole (200-800 mg/d)
      Itraconazole 200 mg BID
      Amphotericin B 0.3-0.5 mg/kg/day
      Capsofungin 50mg IV QD
      Duration of Therapy
      7-14 days or until disease resolution
    • 86. Oral Candidiasis: Treatment
      Relapsing Disease
      Intermittent therapy vs. chronic suppressive treatment
      Decreased azole resistance with chronic suppression vs. intermittent therapy if recurrences are very frequent.
      Avoid maintenance therapy unless relapses are frequent – increased azole resistance
    • 87. Oral Hairy Leukoplakia
      Caused by Epstein-Barr Virus infection
      Does not scrape off with tongue blade
      NOT a premalignant condition
      Targeted therapy not recommended
      Responds to HAART
    • 88. Oral Hairy Leukoplakia
      Linear white patches at edge of tongue. Do not scrape off.
    • 89. Oral Ulcer Diseases
      Several Etiologies
      Most Important Differential Diagnoses:
      Herpes Simplex Virus
      Cytomegalovirus
      Aphthous Ulcers
    • 90. Herpes Simplex Virus
      Multiple vesicular lesions of lips, buccal mucosa, soft palate
      Diagnosis often clinical, also may diagnose by Tzanck smear, viral culture, immunofluorescence assay
      Treatment recommended in patients with HIV
    • 91. Herpes Simplex Virus
      Multiple ulcers with some confluence of buccal mucosa
    • 92. Herpes Simplex Virus
      Tzanck smear with multinucleated giant cells
    • 93. Herpes Simplex Virus:Treatment
      Oral Therapy:
      Acyclovir 400 mg 5x/day 14-21d
      Famciclovir 500 mg BID x 7d
      Valacyclovir 1g PO BID x 7d
      Parenteral Therapy (severe disease)
      Acyclovir 5mg/kg q 8 hours
      Foscarnet or Cidofovir
      for acyclovir resistant disease
    • 94. Cytomegalovirus (CMV)
      Visually indistinguishable from HSV oral ulcer disease
      Often associated with other systemic manifestations of CMV (esophagitis, colitis, retinitis)
      Usually diagnosed in “HSV” refractory to therapy
      Viral Culture/ cytology, IFA, CMV serum antigen testing, CMV PCR
    • 95. CMV Oral Ulcers
      Viral swab demonstrated typical “owl’s eye” intracytoplasmic inclusions. CMV PCR (+)
    • 96. CMV - Treatment
      Limited oral ulcer disease management unclear, but likely a precursor to manifestation at other site (esophagitis, colitis, retinitis)
      Induction Therapy
      Ganciclovir 5mg/kg IV Q 12 hours
      Valganciclovir 900 mg BID
      Foscarnet 90 mg IV Q 12 hours
      Cidofovir 5 mg/kg IV q week PLUS
      Probenecid (to decrease renal toxicity)
      Each then followed by suppressive treatment
    • 97. Aphthous Ulcers
      Present as crops of ulcers from 1-2 mm to 2-3 cm
      Painful lesions lead to odynophagia, dysphagia, secondary weight loss
      Can involve esophagus, other parts of GI tract
      Visually similar to HSV and CMV
    • 98. Aphthous Ulcers
      1.5 cm ulcer of buccal mucosa
    • 99. Aphthous Ulcers
      Diagnosis:
      viral studies for HSV, CMV (-)
      Biopsy: nonspecific inflammatory changes
      Treatment
      Anesthetic mouth washes
      Topical fluocinonide 0.05%
      SEVERE DISEASE
      Prednisone 40 mg/day 4-6 weeks
      Thalidomide 200 mg po QD
    • 100. Kaposi’s Sarcoma
      Can involve any portion of the GI tract.
      Usually symptomatic if oral lesions or intestinal obstruction
      Associated with HHV-8 infection
    • 101. Oral Kaposi’s Sarcoma
    • 102. Kaposi’s Sarcoma
      Presentation:
      Usually in patients with CD4 <200 cells/mm3
      Skin most common site of involvement, but GI tract involved in 40% of visceral cases
      Diagnosis
      Usually based on pathologic specimen
      Must be distinguished from Bacillary Angiomatosis (Bartonella Henselae)
    • 103. Kaposi’s Sarcoma: Treatment
      Often improves with HAART
      Localized Disease
      HAART
      Sclerotherapy
      Intralesional Chemotherapy
      Cryotherapy
      Radiation therapy
      Widespread
      Systemic Chemotherapy
      interferon-alfa ,etoposide, vincristine, vinblastine and bleomycin
    • 104. AIDS Cholangiopathy
      Late manifestation of HIV
      CD4 < 100 cells/mm3
      May be present with or without papillary stenosis
      Clinical Presentation
      Fever, RUQ pain, nausea, vomiting. Weight loss
      Markedly Elevated Alkaline Phosphatase
      Causes Include:
      Cryptosporidium, CMV, microsporidia
      40% of cases – no clear etiology
    • 105. AIDS Cholangiopathy
      Diagnosis
      Ultrasound: may be normal or show intra- and extra-hepatic ductal dilatation
      ERCP: allows imaging of biliary ductal system, sampling of fluid for culture and cytology
      Treatment
      Sphincterotomy for papillary stenosis, biliary stents, targeted therapy at causative agent (if identified)
    • 106. Diarrhea in HIV/AIDS
      Occurs in 50-60% of AIDS patients
      Evaluation should include travel history, pets, medications, foods
      Stool studies
      Stool culture for Shigella, Salmonella, E. Coli, campylobacter
      Stool O&P, acid fast staining
      C. Difficile Toxin Assay
      If Fever: Blood Culture, AFB blood Culture, CMV Antigenemia/ PP65
    • 107. Salmonella
      Commonly S. typhimurium, S. enteritidis
      20-100 greater incidence in AIDS
      Bacteremia common
      Recurrent bacteremia – AIDS defining
      Diagnosis: stool and/or blood cultures
      Treatment: ciprofloxacin, ceftriaxone, amoxicillin, TMP/SMX
      Suppressive Therapy: consider for recurrent disease
    • 108. Shigella
      S. flexneri, S. dysenteriae
      Presentation: bloody diarrhea, fever, abdominal pain
      Complications: megacolon, perforation, bacteremia (50%)
      Treatment: Same as salmonella
      ciprofloxacin, ceftriaxone, amoxicillin, TMP/SMX
    • 109. Clostridium Difficile
      Approximately 8% of AIDS diarrhea
      Diagnosis:
      Detection of toxin in stool
      Thickened bowel wall on CT
      Pseudomembrane on colonoscopy
      Treatment
      Metronidazole 250 mg po QID x 10-14 days
      Vancomycin 125 mg po QID x 10-14 days (if failure of metronidazole)
    • 110. Mycobacterium Avium Complex
      Usually seen with CD4 <100 cells/mm3
      Presentation: fever, abdominal pain, diarrhea, weight loss
      Diagnosis
      Culture: stool, tissue, blood
      CT scan: hepatosplenomegally, abdominal lymphadenopathy
      Treatment
      Clarithromycin 500 mg BID OR azithromycin 500 mg po QD
      PLUS ethambutol 15-20 mg/kg/day
    • 111. Cryptosporidium
      Found in stool of 10-20% of AIDS patients with diarrhea
      Acquired via contaminated water or fecal-oral route
      May also cause biliary tract disease
      Diagnosed by acid fast stain of stool, immunofluorescence
    • 112. Cryptosporidium
      Acid-fast stain of stool demonstrating oocysts
    • 113. Cryptosporidium: Treatment
      Mainstay is restoration of immunity with HAART
      Specific Therapy (disappointing efficacy)
      Paromomycin 1500-2000 mg/d x 14-28 days then 500 mg BID
      Paromomycin 1 g BID PLUS Azithromycin 600 mg QD x 28 days THEN Paromomycin alone
      Octreotide 50-500 units SQ TID
      Reduces stool volume
      Nitazoxanide 500 mg BID
      Currently under clinical trial
    • 114. Isospora Belli
      Acid Fast protozoan
      Symptoms: watery diarrhea, weight loss, cramps
      AFB of stool; larger than cryptosporidium; typical elliptical shape
      Treatment: TMP/SMX DS po QID x 10 days
      Pyrimethamine (for sulfa allergy)
    • 115. Isospora Belli
      Oocyte on modified acid-fast stain of stool
    • 116. Microsporidia
      2 species implicated in most diarrheal disease in AIDS
      Enterocytozoon bieneusi
      Encephalitazoon intestinalis
      Found in 5-50% of AIDS patients with unexplained diarrhea
      Clinical: chronic non-bloody diarrhea, malabsorption, cholangitis, cholecystitis
    • 117. Microsporidia
      Diagnosis
      stool modified trichrome or chemofluorescent staining
      Small bowel biopsy
      Treatment:
      Albendazole 400-800 mg PO >21 days [for E. septata]
      E. bieneusi – limited efficacy
      Metronidazole, atovaquone
    • 118. AIDS Wasting Syndrome
      Unintentional Loss of 10% of body weight
      AIDS defining illness in 15-20% of cases
      Contributing factors:
      Medication related anorexia, depression, oral/esophageal disease, malabsorption
    • 119. AIDS Wasting Syndrome
      Treatment
      Nutritional Supplements
      Oral supplements usually adequate
      TPN for excessive diarrhea from cryptosporidiosis
      Appetite Stimulants
      Megestrol, Dronabinol – weight gain mostly fat
      Resistance Exercise
    • 120. AIDS Wasting Syndrome
      Anabolic Steroids
      Most weight gain is lean body mass (anabolic>androgenic effect)
      Nandrolone
      Oxandrolone
      Oxymetholone
      Testosterone
      Indicated for hypogonadism with or without wasting
      Improved quality of life, libido, energy, lean body mass
    • 121. Non TB Mycobacteria
      MAC rarely cause pulmonary disease
      M.kansasii most common
      CD4< 50
      Interstitial / lobar pneumonia
      Nodules, cavities, adenopathy
      Diagnosis: Cx from respiratory specimen
      Treatment: RIF/ETB/INH 15-18 mo
    • 122.
    • 123. CMV Pneumonias
      Most important AIDS associated viral pulmonary pathogen
      Late
      B/L interstitial/alveolar infiltrates
      Diagnosis:
      CMV culture( not specific)
      CMV inclusions
    • 124. CMV: Treatment
      GCV 2.5 mg/kg Q 8h x 20 d or Valgancyclovir 900 mg BID
      + IVIG 500mg/kg QOD x 10 days
      then GCV 5 mg/kg/d x3-5/wk + IVIG 500mg/kg 2x/wk x8 doses
      Foscarnet 90 mg/kg IV Q 12h x 14-21 days
      then 90 mg/kg QD maintenance
      Cidofovir 5 mg/kg IV Q wk w/ probenecid
    • 125.
    • 126.
    • 127.
    • 128. Pulmonary Cryptococcosis
      Inhaled pathogen
      <15% develop pneumonia
      UL lesions, lobar, B/L, miliary pneumonia
      Pleural effusion, cryptococcoma
      Cavity: rare
      meningitis primary presentation in HIV
    • 129. Pulmonary Cryptococcosis
      Treatment
      Ampho B 0.7-1 mg/kg/d + 5-FC 25 mg/kg q 6h x 2 wks
      Then Fluconazole 400 mg/d x 10wks
      Suppression 200 mg/d until CD4 > 100
      Surgery for cryptococcoma
    • 130.
    • 131.
    • 132. Pulmonary Penicillosis
      Endemic: SE Asia, China, Manipur State of India
      Thermally dimorphic fungus
      Infiltrates, nodules, cavities, abscess, adenopathy
      Disseminated diseases
      Diagnosis: Fungal Culture
      Treatment: Ampho B Itra, 50% relapse
    • 133.
    • 134. Rhodococcus equi
      GP coccobacilli
      Synergistic hemolysis
      Antagonism : IMP, β-lactam
    • 135. Rhodococcus equi
      TB like syndrome with negative smear
      cavitary/nodular pneumonia
      bacteremia
      ½ extrapulmonary
      2/3 mortality
      Tx: 2-3 drugs
      Vanc, IMP,AMG, cipro, Rifampim, E-mycin
    • 136.
    • 137.
    • 138.
    • 139. Non Infectious Pulmonary Diseases
      KS
      Lymphoma
      Nonspecific interstitial pneumonitis
      Lymphocytic interstitial pneumonitis
      BOOP
      PE
    • 140. TB: Early Clinical Picture
      General complaints:
      non-specific
      excessive fatigue
      weight loss
      anorexia
      irritability
      Symptoms of chronic infection:
      low-grade fever
      night sweats
      vague digestive disturbances
      recurrent headaches
    • 141. TB: Early Clinical Picture
      SPUTUM:
      at first dry, and later productive
      purulent sputum
      hemoptysis
      Pleuritic pain from TB pleurisy with effusion, may be a presenting symptom in early stages
      Cough rarely associated with pulmonary TB in children.
    • 142. Severe Pulmonary TB
      Most INFECTIOUS CASES
      Extensive cavities
      Positive smear
      High bacilli output
      > 10 /HPField or >500,000/ml
      High mortality
      without treatment (75%)
      Very infectious
      50% of close contacts infected
      RAPID evolution
    • 143. Chest Xrays in TB Control
      DIAGNOSTIC EXAMINATION of a suspected case
      EVALUATION OF A CASE during treatment
      BUT not a substitute to SPUTUM EXAM
      only sputum monitors response of MTB to drugs
      only sputum provides early warning about resistance
      BASELINE XRAY at the end of treatment
      Evaluation of a CONTACT or an INFECTED
    • 144. Tuberculin Test
    • 145. Tuberculosis Screening – Skin Tests
      15mm
      Person from LOW prevalence area
      NO medical risk factors
      NO known exposure to TB
      10mm
      Person from HIGH prevalence area:
      Asia, Africa, Latin America ³1%
      MEDICAL RISK factors
      5mm
      CLOSE CONTACTS to infectious TB
      OLD TB LESIONS
      HIV INFECTION
    • 146. TB Treatment
      Start with 4 drugs in all patients
      INH, RIF, PZA and EMB or SM until sensitivities return
      If pan sensitive, D/C EMB or SM
      After 2 months of therapy, D/C PZA
      Continue INH & RIF for 4 more months for total of 6 months
      Must have culture conversion by 2 months
      6 month regimen good for HIV(-) and (+)
      Can use BIW regimen / TIW for HIV (+)
      Monitor adherence and toxicity
      DOT, combination pills for self administered (exceptions)
    • 147. Resistance
      Primary resistance to any of the 4 major drugs (INH, Rif, Emb, Sm) was estimated at 12% in the USA in 1995. It ranged in 1994-97 from a low of 2.0 in the Czech Republic to a high of 41% in the Dominican Republic (Global surveillance for anti-tb drug resistance. NEJM 1998, 338,23).
      Median prevalences were:
      INH 7.3%
      Streptomycin 6.5%
      Rifampin 1.8%
      Ethambutol 1%
      All 4 0.2%
    • 148. Clinical Significance of Resistance
      If pan sensitive>95% chance of cure
      If resistant to INH>90% chance of cure
      If resistant to rifampin>70% chance of cure
      If resistant to INH and RIF~50% chance of cure
      Before chemotherapy~50% chance of cure
    • 149. Causes of Resistance
      Irregular Self Administration with Failure to closely supervise
      Care of patients by non specialists
      Increased immigration
    • 150. Epidemiology of TB and HIV
      Both have afflicted similar populations
      Both are socially stigmatizing
      Globally, TB is the 2nd leading cause of death from an infectious disease (behind HIV)
      TB is the leading cause of death in HIV globally
      Active TB may accelerate HIV replication
    • 151. TB/HIV: Epidemiology
      Thirty-six million HIV infected individuals worldwide
      One-third of them co-infected with MTB
      68%- Sub Saharan Africa, 22%- SEA
      Leading cause of death amongst HIV infected individuals worldwide
      Prevalence of HIV in TB patients (India) 20%
    • 152. TB/HIV: Pathogenesis
      Immunity to MTB partly under control of MHC Class II restricted CD4 cells
      Loss of CD4 cells increases risk of
      Reactivation of latent infection
      Primary infection
      Active TB up-regulates HIV replication, leading to accelerated progression of HIV
    • 153. TB/HIV: Pathogenesis
      Life time risk in HIV negative persons: 10%
      5% within first two years
      5% remainder of their lives
      HIV positive persons have 8% risk per year
      HIV+ incidence: 5-16/100 person-years
      Two mechanism
      Reactivation
      Re-infection
      Immune reconstitution TB on HAART
    • 154. HIV/TB: Treatment
      Do you need to add higher number of drugs?
      Do you need to prolong duration of therapy?
      Can ARV be used concomitantly with ATT (anti-Tuberculosis Therapy)?
      Is there increased incidence of AE’s?
      Is there increased incidence of MDR-TB?
      Should latent tuberculosis be treated? (international)
    • 155. Laboratory Testing
    • 156. Serologic Tests
    • 157. Baseline Laboratory Tests
      CD4 count and viral load to establish the stage of the disease
      Exposed other infectious diseases
      Other recommended baseline tests include:
      Hep B and C
    • 163. Laboratory features
      Leukopenia and lymphopenia initially, then lymphocytosis.
      Elevated CD8 cells, decreased CD4 cells.
    • 164. Diagnosis of Acute HIV
      Seroconversion usually occurs within 4 –10 weeks (median 63 days).
      Plasma viral load peaks in three weeks post-exposure (100,000 – 1,000,000 copies RNA/mm3) and then declines to nadir at ~120 days.
      p24 antigen levels may be as high as 100 pg/ml.
    • 165. Management of HIV infection
      MOHD HANAFI RAMLEE
    • 166. Medical and Nursing Care
    • 167. Clinical Care
      (medical & nursing)
      VCT , PMTCT
      preventive therapy (OIs, TB)
      management of STIs and OIs
      palliative care, nutritional support
      antiretroviral therapy
      Socioeconomic Support
      Psychosocial Support
      counseling
      material support
      orphan care
      economic security
      n
      community support services
      food security
      p
      spiritual support
      o
      Human Rights & Legal Support
      r
      stigma & discrimination reduction
      e
      i
      succession planning
      PLHA participation
      v
      e
      n
      Adults and Children
      Affected by
      HIV/AIDS
      t
    • 168. Stage of Management
    • 169. Mx 1 – Risk Assessment
      full history + detailed sexual + drug history
      physical examination  stage
      Initial laboratory tests will include:
      a. A Full Blood Count with differential count, particular attention to be given to platelet and Iymphocyte counts
      b. A Mantoux Test with 1 Tuberculin unit intradermally
      c. A Chest Radiograph
    • 170. Mx 2 – Establish Diagnosis
      HIV antibody Testing:
      ELISA and or Particle agglutination tests
      Confirmed by supplementary test
      a. voluntary basis
      b. anonymously or
      c. confidential basis
    • 171. Mx 3 – Ascertain Stage
      to assess progression of the disease is by measuring the CD4+ Tlymphocyte count and percentage.
      recommended  all HIV infected individuals should have a baseline CD4+
      Infants born  ELISApositive.
      If the infant is not HIV infected  ELISA fall within 18 months after birth.
      Therefore, a better indicator of HIV infection in an infant younger then 18 months will be the measurement of p24 antigen, by doing a polymerase chain reaction (PCR) test, or detection of the virus itself
    • 172. SPECTRUM OF HIV
      MohdHanafiRamlee
    • 173. Group 1 HIV disease (acute seroconversion illness)
      Acute neurological disease
      meningitis
      encephalitis
      olyneuritis
      myelopathy
      brachial neuritis
      GuillianBarre syndrome
      2-4 weeks after the initial HIV
      The symptoms include:
      Flu-like illness
      fever
      arthralgia
      malaise
      myalgia
      headache
      photophobia
      maculopapularrash
      GI disturbances and
      neurological manifestations
      lasts 2-4 weeks  low platelet and Iymphocyte counts, and a low CD4+ T-lymphocyte counts, with a reversed CD4+/CD8+ ratio.
      In the asymptomatic phase the CD4+ Tlymphocyte counts will rise to almost normal levels (600-1200/uL).
    • 174.
    • 175. Group 2 Asymptomatic Phase disease
      3-7 years from the initial HIV infection.
      feels and looks well
      CD4+ T-cell counts can be normal.
      counselled
      towards change of behaviour,
      maintain good health and practise behaviour
      prevent further transmission of HIV.
      assessment for antiretroviral therapy
      6-monthly CD4+ T cell count.
    • 176. Symptomatic Phase (Group 3 and 4) disease
      Viral markers
      p24 antigen
      polymerase chain reaction (PCR)
      p24 antibody (babies, health care workers)
      clinical predictors
      herpes zoster (multi-dermatornal)
      oral candidiasis
      oral hairy leukoplakia
      Prolonged fever, might sweets
      Progressive weight loss
      Laboratory predictors of progression to AIDS:
      thrombocytopenia
      falling CD4+ T. cell counts
      high p24 antigen
      Preliminary investigations
      Chest X-ray
      Full blood count and differential count, ESR
      Stool examination for cryptosporidia/ isospora (when diarrhoea is present)
      Blood cultures for MAI/Mtb, Cryptococcus, Salmonella sp.
      Toxoplasma, Cytomegalovirus, Herpes Antibody titres.
      Sputum for PCP
      Immunological markers
      CD4+ T-cell counts
      CD4+/CD8+ ratio
      CD4+ percentage
    • 177. Perinatal HIV Transmission
      Can occur:
      during pregnancy (intrauterine), 25%--40%
      during labor and delivery (intrapartum), 60%--75%
      after delivery through breast-feeding (postpartum).
      In a randomized trial of formula feeding versus breast-feeding, approximately 44% of HIV infection was attributed to breast-feeding
      Risk factors are associated with perinatal HIV transmission
      immunologically or clinically advanced HIV disease in the mother
      high plasma viral load
      maternal injection-drug use during pregnancy
      preterm delivery
      breast-feeding
      No antiretroviral therapy
      HIV subtype
      Obstetric factors : Delivery >4 hours after the rupture of the fetal membranes; maternal infection with another sexually transmitted disease or coinfection with HSV-2 increased risk of HIV transmission; chorioamnionitis
    • 178. Diagnosis of HIV Infection in Newborns
      Nearly all infants born to HIV-infected mothers passively acquire maternal antibody and, antibody will remain positive until age 18 months regardless of whetherthey are infected.
      Definitive diagnosis of HIV infection in early infancy requires:
      nucleic acid amplification (e.g., polymerase chain reaction [PCR]) or viral culture.
      HIV infection is diagnosed by two positive assays (PCR or viral culture) on twoseparate specimens.
      Infant HIV testing should be done as soon after birth as possible so appropriate treatment interventions can be implemented quickly.
      UMMC: PCR quantitative assay
    • 179. HIV: Reproductive and Women’s Health Issues
      Differences in HIV disease between men and women
      Levels of HIV RNA may be lower in women at seroconversion.
      Mean VL becomes similar within 5-6 yrs.
      CD4 may be higher in women.
      Rates of disease progression do not differ
      No changes in treatment guidelines
      Abnormal Pap Smears
      30%-60% Pap smears have cytologic abnormality
      Cervical cancer presents with high grade pathologic features
      - Uniform relapse after therapy (prior to HAART)
      - Short survival
      HAART has been independently associated with regression of cervical disease.
    • 180. NRTI / NNRTI
      Protease inhibitor
      Entry inhibitor
      Receptor inhibitors
      CCR5 or CXCR4
      Integrase inhibitors
    • 181. Immune Reconstitution Syndrome
      Immune Reconstitution Syndrome
      The use antiretroviral therapy resulted dramatic improvement in outcomes typically associated with an increase in CD4+ lymphocytes, reduced HIV viral loads and partial recovery of T-cell–specific immune responses.
      Recovery of immune function correlates with the number of circulating CD4+ cells. It is safe to discontinue prophylaxis (primary or secondary) for a variety of pathogens including Pneumocystis jiroveci, Mycobacterium avium complex (MAC), and Toxoplasma gondii.
      Some patients experience a clinical deterioration following the introduction of potent antiretroviral therapy believed to be related to the restored ability to mount an inflammatory response.
      The incidence of IRS to be 10% to 25%. In patients undergoing simultaneous treatment of HIV infection and tuberculosis, the incidence of IRS has been reported to be 11% to 45%.
    • 182. Diagnosis of IRS
    • 183. MANAGEMENT OF ADVANCED HIV DISEASE
      MOHD HANAFI RAMLEE
    • 184. Antiretroviral Agent: Zidovudine
      Zidovudine (ZDV)
      a nucleoside analogue, when it is phosphorylated inside HIV -infected cell, inhibits reverse transcriptase.
      Usage
      improved survival
      decreases frequency of opportunistic infections
      Improve quality of life
      cuts down length of hospital stay.
      effective against replicating virus
      can inhibit replication of sensitive strains.
      gold standard in HIV management.
    • 185. Zidovudine: When to Start?
      assessment first
      weight
      opportunistic infections
      immunological status
      if the CD4+ counts are below 200/uL,
      Give zidovudine at 500-600mg per day in 2 or 3 divided doses (250mg b.i.d. or 200mg t.i.d).
      If the CD4+ counts are 200 or less,
      chemoprophylaxis against Pneumocystis carinii pneumonia (PCP)
      Close monitoring & Follow up: 1x/2w  1x/3m 1x/36ml
    • 186. Zidovudine: Site effects
    • 187. Commencing Antiretroviral Therapy
      WHEN ?
    • 188. General Goals of Antiretroviral Therapy
      to prolong survival
      decrease morbidity in those infected
      to improve the patient’s quality of life and reduce the burden on his family and the community.
      To promote prevention of transmission
    • 189. Specific Goals of Antiretroviral Therapy
      to suppress HIV replication
      to reduce plasma viral load to below undetectable levels for a maximum duration
      to improve, maintain and prevent the ongoing decline of CD4 cells.
    • 190. Recommendation on when to commence HAART [MSIDC]
    • 191. Selection of Antiretroviral Agents
    • 192. Successful Antiretroviral Therapy: Critical Factors
      Efficacy
      Tolerability
      Convenience
      -
      -
      Adherence
      Successful Therapy
      Durable viral load
      Suppression
    • 193. Antiretroviral Agents in Malaysia
    • 194. Commencing Antiretroviral Therapy
      WHAT ?
    • 195. HAART
      H = Highly
      A = Active SLOWS DOWN
      A = Anti- VIRAL
      R = Retroviral REPLICATION!
      T = Therapy
      3 or more ARVs. Only recommended ARV treatment – for long term effect.
    • 196. What makes ARVs work?
      Function of ARVs  suppress viral replication
      Virus suppressed  immune system recovers
      Immune system recovery means  CD4 count goes up
      CD4 count up no more opportunistic infections
    • 197. Protease Inhibitor
      Integrase Inhibitor
      NNRTI
      NRTI
      Mechanism of Action of ARVs
      Fusion
      Inhibitor &
      Chemokine
      Receptor
      Antagonist
      Illustration by David Klemm
    • 198.
      • Entering
      CD4 cell
      The virus 
       NNRTI
      NVP, Stocrin
      NRTI (nukes) & nucleotide 
      3TC, d4T
       The ‘factory’
      • New virus
      ‘budding’
    • 199. 3. Integration into
      host cell’s nucleus
      4. Reproduction of viral components
      Assembly and release of new viruses
      2. The virus changes
      from RNA to DNA
      How do PIs work?
      1. Attachment to host cell
    • 200. Pharmacokinetics
      Absorption, Distribution, Metabolism, Elimination
      Renal Elimination
      Liver/GI Metabolism
      Phase I: Oxidation (ie, CYP 450 enzymes)
      Phase II: Conjugation (ie, glucuronidation)
      Antiretrovirals
      Many ARVs (and other medications) undergo Phase I metabolism
      Many ARVs increase or decrease activity of CYP450 (Phase I) enzymes
    • 201. CYP 450 Inhibition
      Leads to blocking of the specific CYP 450 enzyme
      If a drug is metabolized by the CYP 450 enzyme that is blocked
       drug concentration
      Example: Ritonavir
    • 202. CYP 450 Induction
      Leads to production of more CYP 450 enzyme
      If a drug is metabolized by the CYP 450 enzyme that is now in high amounts
       drug concentration
      Example: Efavirenz
    • 203. Drug Interaction Potential
    • 204. NRTIs (Nucleoside Reverse Transcriptase Inhibitors)
      Cytidine
      Tymidine
      Adenosine
      Guanosine
      Zidovudine (AZT)
    • 205. NRTIs (Nucleoside Reverse Transcriptase Inhibitors)
      • Note: Lactic acidosis can occur with any NRTIs
      *dose reduce for renal dysfunction
    • 206. NRTIs
      *dose reduce for renal dysfunction
    • 207. NNRTIs (Non-nucleoside reverse transcriptase inhibitors)
    • 208. NNRTIs
      *Pregnancy Class D
    • 209. Protease Inhibitors (PIs):
      Protease enzyme cleaves HIV precursor proteins (gag/pol polyproteins) 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
    • 210. Protease Inhibitors
      X
    • 211. Ritonavir as a PI Booster
      Ritonavir used only to ‘boost’ concentrations of other protease inhibitors
      Dosed 100-200mg QD-BID
      Available as 100mg capsules and tablets
      Side effects: GI upset; hyperlipidemia*; insulin resistance*
      * All PIs except atazanavir alone
    • 212. Lipodystrophy Illustrations
      “Buffalo hump”
      “Central obesity”
      “Facial and peripheral wasting”
    • 213. Protease Inhibitors
      (1) Take with Food (2) Must be refrigerated
      ** All PIs except atazanavir can increase lipids and cause insulin resistance
    • 214. Protease Inhibitors
      (1) Take with Food (2) Must be refrigerated
      ** All PIs except atazanavir can increase lipids and cause insulin resistance
    • 215. Entry Inhibitors:Fuzeon : Enfuvirtide (T-20)
      FDA-approved fusion inhibitor; 36 AA peptide
      Requires 106 steps to manufacture
      Dose: 90 mg sq bid
      side effects:
      injection site rxn, hypersensitivity (rare)
      resistance: changes in gp41 (cell surface protein)
    • 216. Chemokine Receptor Antagonists
      Maraviroc (Selzentry®)
      CCR5 or CXCR4 receptors on cell surface
      Virus will bind to one of the 2 receptors
      Some patients’ virus will bind to either receptor
      Maraviroc blocks viral entry at CCR5
      Dosed 300mg BID
      150mg BID with P450
      inhibitors
      600mg BID with P450
      inducers
      Tropism
    • 217. Integrase Inhibitors
      Raltegravir (Isentress™)
      Dosed 400mg BID (1 tab 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)
    • 218. Integrase Inhibitor
    • 219. Metabolic Dysfunction in HIV-Infected
      Patients on HAART
      HIV INFECTION
      InsulinResistance
      Dyslipidemia
      Body Fat Redistribution
      HAART
      215
    • 220. Toxicities in Summary
      NRTIs: Lactic acidosis
      Zidovudine: Anemia
      Stavudine and Didanosine: Pancreatitis and Peripheral Neuropathy
      Abacavir: Hypersensitivity (can lead to death); ? CVD
      Tenofovir: renal toxicity
      NNRTIs:
      Efavirenz: nervous system side effects; rash
      Nevirapine: rash, liver toxicity
      Etravirine: rash
      PIs: GI effects, increased lipids, increased BG
      Atazanavir: increased bilirubin, PR prolongation
      Indinavir: kidney stones (LOTS of water)
      Fosamprenavir: rash
      Tipranavir: liver toxicity; bleeding
    • 221. How Do We Treat HIV?
    • 222. Antiretroviral Therapy
      DHHS Guidelines
      Last updated December 1, 2009
      www.aidsinfo.nih.gov
      International AIDS Society- 2008
      Hammer, et al. JAMA Aug 6, 2008
      IDSA Primary Care HIV Guidelines-2009
      Aberg, et al CID Sept 1, 2009
    • 223. Factors to Consider for Initial Regimen Selection
      Potential drug interactions
      Pre-treatment CD4+ T cell count
      Gender
      Pregnancy potential
      Patient lifestyle/ social situation
      Co-morbidities
      Adherence potential
      Dosing convenience (pill burden, dosing frequency, food, fluid restriction)
      Potential adverse effects
      HIV Resistance Testing
      DHHS 4/7/2005, http://AIDSinfo.nih.gov
    • 224. Initiating Therapy in Treatment Naïve Patients
      If AIDS-defining illness or CD4 < 350
      Regardless of CD4 count in:
      Pregnancy
      HIV-associated nephropathy
      HBV co-infection
      Recommended if CD4 count between 350 – 500
      Panel split on initiating in CD4 > 500
      Make a lifelong commitment and understand adherence importance
      DHHS 2009 Guidelines
    • 225. Preferred Regimens for Naïve Patients
      • NNRTI-based regimen
      Efavirenz+ tenofovir+ emtricitabine
      • PI-based regimen
      Atazanavir/r + tenofovir+ emtricitabine
      Darunavir/r QD + tenofovir + emtricitabine
      • INSTI-based regimen
      Raltegravir + tenofovir+ emtricitabine
      DHHS 2009 Guidelines
    • 226. HIV Resistance Testing
      Genotypes
      Sequences patient’s virus by blood sample
      Mutations reported as compared to wild type
      Phenotypes
      Similar to antimicrobial susceptibility testing
      Reports IC50 for patient’s virus
      Compares to wild type virus
      Virtual Phenotypes
      Often reported along with genotypes
      Information obtained from a database of genotypes and matching phenotypes
      An estimate of patient’s phenotype
    • 227. Summary
      HIV infection rates are not declining
      Combination Therapy is CRITICAL
      100% Adherence is ABSOLUTELY NECESSARY
      Drug Interactions are ANTICIPATED
      Adverse Effects occur often
      Some can be managed
      Some are dangerous
      If any doubt, call the physician or ME!

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