HIV/AIDS Flashcards

Question

HIV TREATMENT FAILURE

Answer 1

 Treatment failure can be:  Clinical: Treatment failure should be considered when clinical symptoms appear whilst on therapy that is suggestive of deteriorating status.  Immunological: treatment failure is indicated by a drop of CD4 values to below pre-treatment levels or 50% from the peak value on treatment or perisistant CD4 levels below 50 cells/mm3 after 12 months on therapy. Note: patients initiating at very low CD4 may not be able to mount an adequate CD4 recovery in this case viral load is indicated.  Virologic: plasma HIV viral load >400 copies/ml after 6 months on therapy.  Patients who appear to be failing on treatment while viral load is undetectable should be considered to have undiagnosed opportunistic infection or other concomitant illness.  It should not be concluded on the basis of clinical criteria, that an ARV regimen is failing until there has been a reasonable trial of 1st line therapy lasting at least 6 months, adherence has been assessed and optimized, intercurrent OIs have been treated and resolved and IRIS has been excluded.  Clinical events that occur before the first 6 months of therapy are excluded from this definition because they often represent immune reconstitution inflammatory syndroems related to pre-existing conditions.  Factors leading to treatment failure:  Poor adherence to treatment  Prior exposure to antiretroviral treatment with development of resistance  Primary viral resistance (infected with resistant HIV strain)  Inadequate drug absorption  Suboptimal dosing (e.g. sharing dose because of side effets)  Inadequate or inconsistent drug therapy  Drug interactions

Answer 2

 CD4 count: measures the degree of immune compromise and predicts the risk of opportunistic infections  HIV viral load: measures HIV replication rate, gauges the efficacy of antiretrovirals and predicts CD4 count decline.

Answer 3

Selection of the appropriate combination is based on:  Avoiding the use of 2 agents of the same nucleoside analogue  Avoiding overlapping toxicities and genotypic and phenotypic characteristics of the virus  Patient factors such as disease symptoms and concurrent illnesses  Impact of drug interactions  Ease of adherence to the regimen

Answer 4

 Common side effects of antivirals: GI upset (diarrhea, vomiting, hepatitis especially with Nevirapine), Skin (mild rash, in rare cases hypersensitivity or SJS/TEN), Metabolic (lipodystrophy- fat reduction peripherally i.e. head and limbs but gain central it is seen with NRTIs and PIs; diabetes and dyslipidemia especially with PIs but possible with all)

Answer 5

 These are prodrugs (chain terminators). They use non-specific kinases to be activated (and so carry a risk of bone marrow suppression).  They are used with protease inhibitors (PIs) in HAART

Answer 6

 Drugs:  Zidovudine (azidothymidine)- (AZT)  Tenofovir (TDF)  Abacavir (ABC)  Lamivudine (3TC)  Emtricitabine (FTC)  Stavudine (D4T)  Didanosine (DDI)

Answer 7

 Mechanism of action: NRTIs are analogs of native ribosides (nucleosides or nucleotides containing ribose) which all lack a 3’ hydroxyl group. Once they enter cells, they are phosphorylated by cellular enzymes to the corresponding triphosphate analog which is preferentially incorporated into the viral DNA by reverse transcriptase. Because the 3’ hydroxyl group is not present, a 3’5’ phophodiester bond between an incoming nucleoside triphosphate and the growing DNA chain cannot be formed and DNA chain elongation is terminated.

Answer 8

 Resistance occurs by mutations (multiple) in the gene (pol gene) that codes for reverse transcriptase, integrase and aspartate protease.  Not complete cross-resistance between NRTIs. Mutations confers a high degree of resistance to lamivudine and emtricitabine but more importabtly restores sensitivity to zidovudine and tenofovir.  Because cross-resistance and antagonism occur between agents of the same analog class (thymidine, cytosine, guanosine and adenosine), concomitant use of agents with the same analog target is contraindicated (e.g. Zidovudine and stavudine are both analogs of thymidine and should not be used together)

Answer 9

 Common combinations  First line combinations o Lamivudine/tenofovir (3TC/TDF) o Emtricitabine/tenofovir (FTC/TDF) o Abacavir/Lamivudine (ABC/3TC)  Second line combination: Lamivudine/ zidovudine (3TC/ AZT)  Others: didanosine, stavudine

Answer 10

 These do not require activation by cellular enzymes to inhibit reverse transcriptase inhibitor. (they are not prodrugs, no risk of myelosuppresion)  They are additive or synergistic with NRTIs

Answer 11

 Drugs:  Efavirenz (EFV) o Can disrupt sleep cycle (insomnia and “dysphoric dreams”-nightmares) and cause psychosis o Avoid in pregnant women  Nevirapine (NVP) o A single dose of NVP given at the time of delivery will decrease vertical transmission of HIV by 50%. o Primary side effects: Rash and increased liver function tests (hepatotoxicity) as well as Stevens-Johnson syndrome and Toxic epidermal necrolysis o It is an inducer of cytochrome P450 3A4 and so shows drug interactions (i.e. with warfarin)

Answer 12

 Mechanism of action  Aspartate protease (pol gene encoded) is a viral enzyme that cleaves precursor polypeptides in HIV buds to form the proteins of the mature virus core  Enzyme contains a dipeptide structure not seen in mammalian proteins. PIs bind to this dipeptide inhibiting the enzyme  Resistance occurs via specific point mutations in pol gene such that there is not complete cross-resistance between different PIs

Answer 13

 Drugs:  Lopinavir/ritonavir (LPV/r): due to poor bioavailability it is boosted with ritonavir  Saquinavir (SQV): one of the least toxic and has low oral bioavailabity and so is also boosted with low dose ritonavir  Ritonavir (RTV): no longer used as a single PI but used as a booster of other PIs  Indinavir (IDV): combined with ritonavir nearly always in combination regiemns with 2 NRTIs  Atazanavir (ATV)  Darunavir (DRV)

Answer 14

 Side effects:  Crystalluria (indinavir)  Syndrome of disordered lipid and carbohydrate metabolism with central adiposity and insulin resistance (less with atazanavir)  Gall stones (atazanavir)  Kidney stones (indanavir)

Answer 15

 Major drug interactions (Ritonavir works on cytochrome P450) o Rifampicin o Digoxin (use lower dose of digoxin dose) o Oral contraceptives: use higher dose contraceptives

Answer 16

 Drugs:  Enfuvirtide (fusion inhibitor)  Maraviroc (Entry inhibitor-CCR5 inhibitor)

Answer 17

 Inhibit intergrase preventing integration of viral genome into host genome  Drugs:  Dolutegravir  Raltegravir

Answer 18

 Cross-resistance between raltegravir and elvitegravir can occur although dolutegravir has limited cross-resistance to other integrase inhibitors.

Answer 19

 Side effects: nausea, diarrhea are most common as drugs are well tolerated.

Answer 20

 PrEP is used as a preventive measure of HIV transmission in people at substantial risk of HIV acquisition.  Eligibility criteria:  No suspicion of acute HIV infection  Test HIV negative  Perceives to be at substantial risk of HIV acquisition and willing to be adherent  Able to attend regular 3 month reviews and HIV testing  Able to concomitantly apply other methods such as barriers to prevent the transmission of other STIs  Willing to stop taking PrEP when no longer eligible  People at high risk: engaging in 1 or more of the following in last 6 months o Vaginal/anal intercourse without condomes with more than 1 partner o Sexually active with a partner who is known positive or at substantial risk of being HIV positive o Sexually active with an HIV positive partner who is not on effective treatment (ART for <6 months or not virally suppressed) o History of STI o History of PEP use o Sharing injection material or equipment

Answer 21

 ARVs are used for oral PrEP and PEP  Oral PrEP containing Tenofovr disoproxil fumarate (TDF) or alternatively Tenofovir alafenamide (TAF) with with either Emtricitabine (FTC) or Lamivudine (3TC) should be offered as an additional prevention choice for people at substantial risk of HIV acquisition as part of combination HIV prevention approaches.  Drugs used:  TDF + XTC (emtricitabine FTC or lamivudine 3TC) is safe in pregnancy and during breastfeeding. It is also active against hepatitis B infection thus discontinuation of this combination requires close monitoring in those infected with hepatitis B due to concern of rebound viremia  TAF + FTC can be used in patients with a Creatinine clearance between 30 and 50ml/min, though TAG is not currently recommended for use in patients with TB or pregnancy.

Answer 22

 Persons with osteopenia/Osteomalacia/osteoporosis may be at risk of bone loss associated with TDF therefore TAF would be recommended in such population  TDF should not be co-administered with other nephrotoxic drugs e.g. aminoglycosides.  Standard TB medication or oral contraceptives do not interact with PrEP drugs and there is no need for dose adjustments.  PrEP clients must be routinely test for HIV infection and ART offered immediately if the PrEP user seroconverts.  PrEP should be taken a minimum of 7 days in men and 21 days in women to achieve maximal protection from HIV acquisition before engaging in high risk sexual exposure and must be continued as long as risky exposure persists or one remains negative.  PrEP should be discontinued after 4 weeks of elimination of the risky exposure.  Note: PrEP alone is not 100% effective at preventing HIV and clients need to be counselled that they should use other prevention methods as well

Answer 23

 This is the use of ART to prevent HIV transmission.  There is no risk of transmission when the skin is intact.  Factors associated with increased risk:  Deep injury  Visible blood on the device that caused the injury  Injury with a large bore needle from artery or vein  Unsuppressed HIV viral load in source patient  Body fluids and materials that pose risk of HIV transmission are amniotic fluid, cerebrospinal fluid, human breast milk, pericardial fluid, peritoneal fluid, pleural fluid, saliva in association with dentistry, synovial fluid, unfixed human tisues and organs, vaginal secretions, semen, any other visibly blood stained fluid and fluid from burns or skin lesion.  Management:  Immediately after exposure o Clean the site: wash skin wounds with soap and running water. Do not squeeze, allow wound to freely bleed. If the exposed area is an eye or mucous membrane, flush with copious amounts of clean water. Do not use bleach or other caustic agents/disinfectants to clean the skin  Contact incharge or supervisor  Consult medical officer to determine the need for PEP based on the risk of transmission and risks and benefits of taking (or not taking) ART

Answer 24

 This may occur at any time in the course of HIV infection, most commonly at the time of acute HIV infection.  It becomes increasingly rare following the development of AIDS.  Patients experience a syndrome of:  Headache  Photophobia  Sometimes: Frank-encephalitis and cranial nerve involvement (Commonly VII cranial nerve is affect)  CSF findings:  Lymphocyte pleocytosis 10-100 cells/L  Increased protein level  Normal glucose level  Diagnosis of HIV: HIV serology may be negative if it occurs during the primary HIV infection. To confirm the diagnosis of HIV p24 antigen or DNA PCR may be done or repeat serology after few weeks.  The syndrome usually resolves spontaneously within 2-4 weeks.

Answer 25

 This may be the first AIDS defining illness in up to 5-10%. It is a major cause of dementia in young people.  A major feature of this entity is the development of dementia which is defined as a decline in cognitive ability, motor and behavioral dysfunction.  Triad:  Cognitive dysfunction  Motor dysfunction  Behavioral dysfunction  Diagnosis:  Neuropsychological tests  Mini-mental test  It is often a diagnosis of exclusion  Treatment:  Antiretroviral therapy especially with those that penetrate the CNS (zidovudine, Stavudine, abacavir and nevirapine)  Supportive care

Answer 26

 Occurs in 1/3 of patients with AIDS.  Types:  Mononeuropathy e.g. Bell’s palsy  Mononuritis multiplex  Distal sensory peripheral polyneuropathy (DSPN)  DSPN: is the most common, it presents with symmetric bilateral painful burning sensation, paresthesia and tingling of the feet and lower extremities.  Diagnosis:  Clinical  Nerve condution study  Exclsion of other causes  Treatment: Symptomatic treatment and discontinuation or changing the drug causing it when symptoms are severe.

Answer 27

 These are a relatively frequent complication of HIV infection.  They may be due to opportunistic infections, neoplasms or HIV encephalitis.  The seizure threshold is often lower than normal in patients with HIV infection owing to the frequent presence of electrolyte abnormalities.  CNS infections may cause increased released of ADH (SIADH) with reabsorption of water and a Euvolemic hyponatremia.  Common causes:  CNS toxoplasmosis  Primary CNS lymphoma  Cryptococcal meningitis  HIV encephalopathy  Treatment:  Most of the time patient will have 2 or more seizures suggesting that anticonvulsant therapy is indicated in all patients with HIV infection and seizures unless a rapidly correctable cause is found.  While phenytoin (100mg PO TDS) remains the initial treatment of choice. Phenobarbital (100mg PO every night) or Valproic acid are aslo alternative.

Answer 28

 Common etiological agents: S. pneumoniae.  As the degree of immunosuppression worsens pneumonia may be recurrent and associated with sepsis  Clinical presentation:  Abrupt onset fever  Cough  Production of purulent sputum  Dyspnea  Pleuritic chest pain  Recommended investigations:  Chest Xray: o Pneumonic consolidation o Infiltrate o Pleural effusions  Blood culture  FBC: leukocytosis  Gram stain of the sputum  Sputum culture and sensitivity  Treatment:  Antibiotics: Penicillin (procaine Pen/Crystalline Pen), Amoxicillin, Fluoroquinolones  Supplemental oxygen

Answer 29

 This is caused by a fungus Pneumocystis jiroveci.  It is one of the commonest OIs in industrialized countries however, due to initiation of antiretroviral therapy and use of CTX prophylaxis its incidence has declined.  50% of patients experience at least one bout of PCP during the course of their life time.  It is transmitted from human to human or from environmental reservoirs to human.

Answer 30

 Indolent course characterized by weeks of vague symptoms prior to presentation or diagnosis.  Median duration of symptom is 28 days.  Dyspea and fever are cardinal symptoms  Cough with scanty sputum in more than 2/3 of cases  Physical examination reveals: (findings may be minimal, usual findings or pneumonia may not be noted) o Respiratory distress +/- cyanosis o Little abnormality on chest examination: rhonchi or wheeze may be heard especially in patients wiith some other underlying pulmonary disease; findings of consolidation are usually absent. o P. jiroveci appears to be capable of hematogenically spread with seeding of a variety of organ systems as well as causing primary infection of the ear

Answer 31

 Chest X-ray: could be normal or show diffuse bilateral alveolar/interstitial infiltrates.  LD is elevated in more than 90% cases: has a very high negative predictive value i.e. if LDH level is low in a patient the diagnosis of PCP is less likely.  Definitive diagnosis- demonstration of the trophozoite or cyst from the organisms in camples obtained from induced sputum in which the yield is 60% or Broncho-alveolar lavage in which the yield is 95%. Staining: WrightGiemsa, Methenamine silver, Direct IF, PCR.  Other tests: Gallium 67 scan, PFT, ABG

Answer 32

 Antibiotics: o Gold standard: Co-trimoxazole IV/PO o Dose: 15mg/kg/day (trimethoprim) in 3-4 divided doses (3-4 tabs 480mg QID) o Duration of treatment: 21 days (3 weeks) o Side effects: rash, fever, leucopenia o Response to treatment may not occur until the end of the first week and the patient may get worse during the first few days owing to the inflammatory response resulting from the death of large number of organism in the lungs. o Alternatives:  Clindamcin 600mg IV 8 hourly or 300-400mg PO 6 hourly + Primaquine 15-30mg base/day x 21 days  Pentamidine 4mg/kg/day IV x 21 days  Atovaquone 750mg PO BD with meal x 21 days  Adjunct treatment o Supplemental oxygen o Steroids: reduce need for mechanical ventilation and mortality in 50%  Start within 72 hours of presentations  Indications: moderate/severe respiratory distress or cyanotic (PaO2 <70mmHg)  Dose: Prednisolone 40mg PO BD x 5days, 40mg PO daily for 5 days, 20mg PO daily for 11 days  PCP prophylaxis o Primary prophylaxis:  Recommended for HIV infected persons with evidence of significant immune deficiency  CD4 <200/microliter  HIV associated thrush  Unexplained fever o Secondary prophylaxis: for patients with prior episode of PCP o Regimens:  TMP-SMX 2 tablets/day (single strength)  TMP-SMX 2 tables three times a week o Alternatives  Dapsone 100mg PO daily  Dapsone 50mg PO daily plus pyrimethamine 50mg PO weekly plus folinic acid 25mg PO weekly  Aerosolized pentamidine 300mg monthly via nebulizer  Atovaquone 1500mg daily o Prevention of PCP may also be beneficial in reducing the risk of having other HIV associated infections such as CNS toxoplasmosis and other bacterial infections.

Answer 33

 This is due to infection with Candida albicans.  It can manifest as:  Oral candidiasis o Appears as white, chessy exudates, often on an erythematous mucosa (most commonly seen on the soft palate) which gives an erythematous or bleeding surface on scrapping o Erythematous form: there is predominantly erythema rather than white patches  Esophageal candidiasis o Usually coincides with CD4 count of <50/L o Causes substernal pain or a sense of obstruction on swallowing o Most lesions occur on the distal third of the esophagus and appears on endoscopy as redness, edema and focal white patches or ulcers. o If an HIV infected person has oral thrush and substernal pain on swallowing presumed diagnosis of esophageal candidiasis can be made. o Endoscopy is needed to prove the diagnosis but is unnecessary if the patient responds to antifungal therapy o Linear ulcerations of the esophagus may be seen on barium X-ray

Answer 34

 Oral candidiasis: o Nystatin IU/ml suspension 2.5-5ml gargled 5times daily o 2% Miconazole oral gel applied 2-3 times daily o Amphotericin B lozenges o Fluconazole 100-200mg PO/day for 7-14 days in severe and persistent cases o Oral hygiene, discontinue steroids and antibiotics if the patient is taking any.  Esophageal candidiasis: Fluconazole 200mg/day PO (up to 400mg/day) for 14-21 days

Answer 35

 This is characterized by white plaques with vertical ridging on the sides of the tongue.  Unlike with oral Candida the lesions cannot be peeled off.  It was first recognized in HIV disease but can rarely occur in other forms of immunosuppression.  It is thought to be due to co-infection with Epstein-Barr virus.  Treatment is with acyclovir, ganciclovir or foscarnet.

Answer 36

 This is a common clinical condition in over 50% of HIV infected patients  It may be acute or chronic, watery, mucoid or bloody  It may or may not be associated with fever.  Spectrum of condition varies with degree of immunodeficiency state.

Answer 37

 Pathogens may be:  Bacterial  Viral  Protozoal  Fungal  Spirochetal  Mycobaterial  Metazoa  Others (malignancies)

Answer 38

 Mechanism of diarrhea:  Adhesion to mucosal surface  Enterotoxin  Entero-invasion  Atrophy of mucosal

Answer 39

 This is diarrhea lasting for more than 2 weeks with a single watery bowel motion and/or 3 or more loose stools per day.  Frequency of diarrhea increases as the CD4 count falls  With Antiretroviral therapy, incidence of chronic diarrhea decreases  Protozoa causing chronic diarrhea: o Cryptosporidium parvum o Isospora belli o Microsporidium

Answer 40

 HIV enteropathy (AIDS enteropathy)  This is a chronic diarrheal syndrome for which no etiologic agent other than HIV can be identified (Chronic diarrhea of unknown cause).  Clinical features o Early stage: intermittent self-limiting diarrhea however in advanced stage, persistent life threatening diarrhea o Copious amount of stool several times per/day associated with abdominal cramp, nausea and vomiting o Significant weight loss (wasting) may occur due to the associated malabsorption o Fluid and electrolyte depletion

Answer 41

 Stool microscopy, culture and sensitivity  Special stains: Modified AFB stain (Modified ZN stain)  Intestinal biopsy

Answer 42

 General treatment of chronic diarrhea  Hydration: oral, parenteral with electrolyte replacement  Symptomatic treatment: Anti-diarrheal agents o Loperamide 2-4mg QID o Lomotil 5mg QID o Tincture of opium 0.3ml QID o Codeine tablets  Specific treatment  Cryptosporidium o Nitazoxanide 0.5-1.0g BD or o Paromomycin 1g BD + Azithromycin 600mg QID  Isospora o Cotrimoxazole 2 tabs QID for 10 days then BD for 3 weeks or o Pyrimethamine 75mg + Folinic acid 10 o Chronic suppression (Secondary prevention) Cotrimoxazole 2 tabs/day or pyrimethamine 25mg + folinic acid 5mg QID

Answer 43

 This is a parasitic infection caused by Strongyloid stercolaris.  It is acquired through skin penetration of its larva form.  Auto-infection is common  In its life cycle there is transition via the lungs and settles in the GIT, primarily small intestine free-living or parasitic.  Usually a mild disease in immunocompetent individuals.  Disseminated infection common in immune-compromised hosts  Systemic manifestation may mimic sepsis.

Answer 44

Clinical manifestations:  Immunocompetent: asymptomatic to mild symptoms with occasional severe pruritus. It may manifest with mild diarrhea, epigastric pain.  Immunocompromised: large amount of filariform larva are released and may invade o GIT tract: causing enteritis with severe diarrhea and malabsorption o Lungs: manifest with cough, shortness of breath (Lofflers’ pneumonia) o CNS, peritoneium and liver may also be invaded o Severe systemic symptoms are commonly seen in disseminated infection o May be complicated by gram negative sepsis

Answer 45

 Treatment:  Ivermectine 200g 1-2 days  Thiabendazole 75mg/kg BD for 3 days  Albendazole 400mg/day for 5 days

Answer 46

 This is a chronic itchy condition commonly seen in HIV infected patients.  Symmetrical non-folliclar papules are seen on the trunk and extensors of extremities.  It is the most common cutaneous manifestations in HIV.  Diagnosis: Biopsy  Treatment:  Topical: Antipruritic lotion, corticosteroid, oatmeal bath  Systemic: Antihistamines, Corticosteroids, Phototherapy, UV-B, UV-A + Psoralen

Answer 47

 This is a tumor of vascular and lymphatic endothelium that presents as purplish nodules and plaques on skin and mucosa.  It was first described by Moritz Kaposi in 1872.  Immunosuppression increases risk of KS 400-500 times higher than general population.  The presence of human herpes virus 8 (HHV-8) is found in all types of KS.  KS has a worldwide distribution. In Africa it occurs largely in the south of the Sahara.  Prevalence of AIDS-related KS has decreased due to widespread availability of HAART.  KS associated with other forms of immunosuppression include those with iatrogenic suppression from oral prednisolone or other chronic immunosuppressive therapies as may be given to transplant patients.  It affects more men than women (2:1 ratio).  It is the most common cutaneous malignancy in HIV disease.  This condition carries a variable clinical course ranging from minimal mucocutaneous disease to extensive organ involvement.  Various visceral organs can also be affected.

Answer 48

 KS is formed by abnormal proliferation of vascular endothelial cells.  Infection with HHV-8 has been associated with the development of KS.  HHV-8 (human herpes virus-8) is found in KS lesional tissue irrespective of clinical type.  Transmission of HHV-8: mainly through saliva, organ transplantation, blood transfusion it is even believed to be transmitted sexually.  HHV-8 titers 2-3 times higher in saliva than in semen, anorectal or prostate fluid samples.  HHV-8 is known to encode products that lead to growth dysregulation or evasion of immune surveillance.  A virally encoded G protein induces VEGF (vascular derived endothelial growth factor) production, stimulating endothelial growth  Cytokines produced by inflammatory cells recruited to the sites of lytic infection also create a local proliferative milieu  Other proteins disrupt normal cellular proliferation and prevent apoptosis by inhibiting p53.  HIV virus Tat protein potentiates the milieu conducive to KS growth

Answer 49

 Can affect almost any organ system.  Cutaneous lesions in Kaposi sarcoma are characterized as follows:  Cutaneous lesions may occur at any location but typically are concentrated on the lower extremities and the head and neck region.  Lesions characterized by brown, pink, red or violaceous macules/patches, papules/plaques, nodules.  Nearly all lesions are palpable and nonpruritic  Lesions may range in size from several millimeters to several centimeters in diameter.  Lesions may assume a brown, pink, red or violaceous color and may be difficult to distinguish in dark-skinned individuals.  Lesions may be discrete or confluent and typically appear in a linear, symmetrical distribution, following Langer lines.  Mucous membrane involvement is common (palate, gingiva, conjunctiva)  Lesions may vary depending on the clinical variant.  Mucous membrane, cutaneous and visceral involvement is common (lymph nodes, GIT and lungs).

Answer 50

 The subtypes of KS include:  Classic or sporadic  African cutaneous (Endemic)  AIDS-associated (Epidemic)  Immunosuppressant therapy related (iatrogenic)

Answer 51

 It is an indolent disease.  It is seen chiefly in middle-aged men of southern and Eastern European origin.  It is not associated with HIV.  Early lesions appear most commonly on the toes or soles as reddish, violaceous or bluish-black macules and patches that spread and coalesce to form nodules or plaques.  Brawny edema of the affected limb may be present  Macules or nodules may appear, usually much later on the arms and hands and rarely may extend to the face, ears, trunk, genitalia or oral mucosa.  Classic KS has a slowly progressive course.

Answer 52

 Endemic in tropical Africa.  Mostly seen in men between the ages of 20 and 50.  It is seen in HIV-seronegative persons.  It has a locally aggressive but systemically indolent course.  Characterized by nodular, infiltrating, vascular masses on the extremities.  A particularly severe form, with prominent lymph node and visceral involvement, occurs in pre-pubertal children, the prognosis is poor, with an almost 100% mortality rate within 3 years. (African lymphadenopathic Kaposi sarcoma)  An aggressive disease of young patients mainly children under age 10.  Lymph node involvement with or without skin lesions.  Has an aggressive course, often terminating fatally within 2 years on onset.

Answer 53

AIDS ASSOCIATED KAPOSI SARCOMA (EPIDEMIC)  KS in patients immunosuppressed by AIDS.  AIDS-related Kaposi sarcoma, unlike other forms of the disease, tends to have an aggressive clinical course.  It is the most common presentation of Kaposi sarcoma.  Cutaneous lesions begin as one or several red to purple-red macules, rapidly progressing to papules, nodules, and plaques.  There is a predilection for the head, neck, trunk and mucous membranes.  A fulminant, progressive course with nodal and systemic involvement is expected.  It may be the presenting manifestation of HIV infection (HIV stage 4).

Answer 54

IMMUNOSUPPRESION-ASSOCIATED KAPOSI SARCOMA  Occurs in patients on immunosuppressive therapy  Clinical features may be similar to that of classic KS, however, site of presentation is more variable.  Removal of immunosuppression may result in regression of the KS

Answer 55

INTERNAL ORGAN INVOLVEMENT  Classic KS: GIT is most frequently involved (intestinal blockage and bleeding). Lungs, heart, liver, conjunctiva, adrenal glands, abdominal lymph nodes, and bones may also be affected.  African cutaneous KS (endemic): frequently accompanied by massive leg edema and frequent bone involvement.  African lymphadenopathic KS: reported among Bantu children who develop massive lymph node involvement, preceding appearance of skin lesions. The children also develop lesions on the eyelids and conjunctiva.  Eye involvement is often associated with swelling of the lacrimal, parotid, and submandibular glands.  AIDS-associated KS: Lungs (37%), Gastrointestinal tract (50%), and lymph nodes (50%).

Answer 56

 Skin and oral lesions can be diagnosed by visual examination even though skin biopsy is most accurate to make diagnosis.  Lung and GI-tract lesions would need endoscopy and biopsy for accuracy.  Resolution of skin lesions with HAART can give a presumptive diagnosis.  Testing for HHV-8 is more research than clinically applicable. WORK-UP  Baseline investigations: Full blood count, Liver enzymes, Urea & electrolytes, Creatinine, RPR (syphilis)  Skin biopsy  Prominent spindle cells  Prominent slit-like vascular spaces  Extravasated red blood cells  Immunohistochemistry  HIV test  HHV-8 PCR  CXR/CT-scan  Endoscopy

Answer 57

 Bacillary angiomatosis  Pyogenic granuloma  Leukemia cutis  Cellulitis  Severe stasis dermatitis  Small-vessel vasculitis

Answer 58

 Topical retinoid (Alitretinoin gel 35-50% response)  Surgical excision  Local Radiation (20-70% response)  Cryotherapy (85% response)  Laser  Anti-retroviral therapy for epidemic KS  Chemotherapy:  Liposomal doxorubicin, liposomal daunorubicin  Vincristine, Bleomycin, Doxorubicin: 1st line at UTH/CDH  Paclitaxel monotherapy: 2nd line agent

Answer 59

 Classic KS: Progresses slowly, rare lymph node or visceral involvement. Death occurs years later from unrelated causes.  African cutaneous KS: Aggressive, early nodal involvement, death from KS expected within 1-2 years.  AIDS-related KS: although widespread, most patients die of intercurrent infection  Immunosuppression related KS: removal of immunosuppression may result in resolution of the KS without therapy.

Answer 60

 Lymphomas occur with increased frequency in immunodeficiency states.  As HIV disease progresses the risk of lymphoma increases.  The incidence of lymphoma has not shown dramatic decrease even after HAART is being widely used by HIV patients worldwide.  It is a late manifestation which often occurs when the CD4 count falls below 200/mm3  3 main categories are seen with HIV  Grade III or IV immunoblastic lymphoma (60%)  Burkitt’s lymphoma (20%)-associated with EBV  Primary CNS lymphoma  Treament:  In patients with high CD4 count- intensive chemotherapy, low dose chemotherapy in patients with low CD count.  Palliative measures to decrease the size of the lesion and associated edema o Radiotherapy o Glucocorticoides

Answer 61

 There is a 5 fold increased risk of developing cervical cancer in women with AIDS.  It is associated with human papilloma virus infection.  Invasive carcinoma of the cervix is an AIDS defining illness  Abnormal PAP smear is seen in 60% of HIV infected women  Anorectal CA may also be seen in homosexual men

HIV/AIDS Flashcards

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