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57 Cards in this Set
- Front
- Back
do most people die from an HIV infection?
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no, they die due to a suppressed immune function and resulting infective illness
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between what CD4 count is a patient at risk for Kaposi's Sarcoma
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~300
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between what CD4 count is a patient at risk for PCP & Herpes simplex
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~200
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between what CD4 count is a patient at risk for oral candidiasis
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300-250
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between what CD4 count is a patient at risk for herpes zoster
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~350-300
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between what CD4 count is a patient at risk for non-hodgkins lymphoma
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250-200
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between what CD4 count is a patient at risk for cryptococcus and toxoplasmosis?
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150-100
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between what CD4 count is a patient at risk for MAC and CMV?
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100-50
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when should one start/stop PRIMARY prophylaxis for PCP?
what about secondary? |
PRIMARY: start CD4<200, stop CD4>200x3mo
SECONDARY: start CD4<200, stop CD4>200x3mo |
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when should one start/stop PRIMARY prophylaxis for toxoplasmosis?
what about secondary? |
PRIMARY: start CD4<100 & IgG+ (+ serology); stop CD4>200x3mo
SECONDARY: start CD4<200; stop CD4>200x6mo |
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when should one start/stop PRIMARY prophylaxis for MAC?
what about secondary? |
PRIMARY: start CD4<50; stop CD4>100x3mo
SECONDARY: start CD4<100; stop CD4>100x6mo |
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when should one start/stop PRIMARY prophylaxis for candidiasis?
what about secondary? |
N/A -- no prophylaxis required, treat as pt acquires it
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when should one start/stop PRIMARY prophylaxis for cryptococcus?
what about secondary? |
PRIMARY: NOT recommended (consider at CD4<50) -- stop: n/a
SECONDARY: CD4<100-200; stop CD4>100-200x6mo |
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when should one start/stop PRIMARY prophylaxis for histoplasmosis?
what about secondary? |
PRIMARY: consider start CD4<50; stop n/a
SECONDARY: life long suppressino |
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when should one start/stop PRIMARY prophylaxis for CMV?
what about secondary? |
PRIMARY: consider start CD4<50; stop n/a
SECONDARY: consider start CD4<100-150; stop CD4>100-150x6mo |
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what is the clinical presentation of PCP?
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pulmonary dysfunction (pneumonia)
early disease: mild sx-mild cough, exertional dyspnea, normal chest x-ray severe disease consistent with BILATERAL pneuml: fever, nonproductive cough, SOB, diffuse pulmonary infiltrates |
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what is the preferred treatment regimen for PCP?
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high dose bactrim (15-20mg/kg/day in 3-4 divided doses) --- 2 bactrim DS tid
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what about corticosteroid use in PCP?
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add on if PO2 <70mmHg
drug: methylprednisone, prednisone |
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if pt has a sulfa allergy, can bactrim still be used for tx of PCP? what are some s/sx of bactrim intolerance?
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sulfa allergy -- do NOT use bactrim
s/sx: fever, rash, neutropenia, anemia, thrombocytopenia, hepatits, pancreatitis, interstitial nephritis |
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if a pt is bactrim intolerant, what are other tx options for PCP?
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dont memorize - just be able to recognize that they are used SECOND line:
clindamycin + primaquine trimethoprim + dapsone atovaquone pentamide |
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what is the preferred regimen for PCP prophylaxis? at what CD4 level should pt undergo chemoprophylaxis?
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bactrim DS or SS po QD or DS TIW (less efficacious)
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How is PCP diagnosed?
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respiratory culture and symptoms
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this disease is associated with undercooked pork, lamb, beef, transplacental spread, and ingestion of cat-derived oocysts
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toxoplasmosis
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toxoplsmosis is manifested via:
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CNS*****: encephalitis, abcess
lung: pneumonitis eye: retinochoroiditis |
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CNS manifestations in pts w/toxoplasmosis are:
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fever, focal neurologic defect
ring enhancing lesions on MRI |
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toxoplasmosis treatment regimen
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pyrimethamine + leucovorin + sulfadiazine x 3-6wks
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why is leucovorin part of the treatment regimen for toxoplasmosis?
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lecovorin is added to decrease pyrimethamine toxicity (its a folic acid savior)
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what about maintenance therapy for toxoplasmosis? how long should the patient be on 3 drug treatment regimen?
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may decrease dosage from treatment regimen for maintenance;
should be in place until CD4 count is restored (to >200x6mo)due to high relapse rate |
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what regimen is used for toxoplasmosis prophylaxis???
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primary: bactrim DS or SS po QD
secondary: maintenance therapy with pyrimethamine+sulfadiazine+leucovorin |
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what should be done before beginning toxoplasmosis prophylaxis?
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1. test IgG to Toxoplasma (T. gondii) to asses previous exposure -- IgG should be +
2. CD4 count should be <100 stop w/CD4>200x3mo with primary prophylaxis |
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What is the clinical presentation of oropharyngeal Candidiasis?
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oral: creamy white patches on the tongue and other mucosal sufaces
pts may experience pn w/subsequent decrease in food and fluid intake esophageal: painful swallowing, obstructed swallowing, sub-stemal pn vulvovaginal: creamy, white abnormal discharge, pruritis, pn, dysuria, dyspareunia |
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pathogen that causes cadidiasis
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Candida albicans
but there are exceptions: dubliniesis, glabrata, kruseii |
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how does treatment differ for mild vs. moderate to severe OPCC?
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mild: topical therapy
moderate to severe, esophagitis: ALWAYS systemic therapy |
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what are the treatment options available for OPC?
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AZOLES: fluconazole**, miconazole, itraconazole, voriconazole
POLYENES: nystatin and amphotericin B ECHINOCANDINS: caspofungin, anidulafungin, micafungin |
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what is the MOA of azoles?
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inhibit fungal CYP450-dependent ergosterol synthesis, resulting in impaired cell membrane integrity
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what is the MOA of polyenes?
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bind to ergosteral and disrupt fungal cell membrane
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what is the MOA of echinocandins?
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inhibit beta 1,3-glucan synthase, disrupting cell wall synthesis
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what are the advantages/disadvantages of using azoles for OPC?
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IV, PO formulations
fewer side effects drug interaction potential |
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what are the advantages/disadvantages of using polyenes for OPC?
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Nystatin is available oral or topical
amphotericin B has MANY ae's including renal dysfunction, infusion reactions, electrolyte abnormalities |
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what are the advantages/disadvantages of using echinocandins for OPC?
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they are safe, avail on IV, and VERY expensive
*used when someone has developed resistance to azoles or poplyenes |
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treatment regimens for THRUSH
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clotrimazole oral troches 10mg 5x/day until lesions resolve
nystatin 500,000units gargled/swich and swallow 4-5x/day fluconazole po 100+mg/day other options = for resistant or unresponsive OPC: itraconazole, voriconazole, oral amphotericin B, IV amphotericin tx until symptoms resovlve (usually 7-14d) |
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treatment regimens for esophageal candidiasis
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do NOT use topical (nystatin, clotrimazole)
Treat systemically for 14 to 21 days (Most pts respond in 5 days; Consider increasing dose or changing agent if response not seen) Fluconazole 200mg/day and up 800mg – 1600mg may be used in certain patients Alternative regimens: Itraconazole, voriconazole, amphotericin B, echinocandins |
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is prophylaxis required for candida? if so - at what CD4 count?
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Primary: Not routinely recommended
Secondary: Consider with history of esophageal candidiasis Fluconazole 100-200mg/day May consider with many repeat occurrences of oral thrush candidiasis is more frequent with CD4<100 |
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diagnosis of candidiasis is made by doing what?
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clinical exam, KOH test
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this OI is caused by inhalation, then hematogenic dissmination of aerosolized organism...which is found in pigeon droppings and nesting places
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Cryptococcus neoformans
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S/SX of Cryptococcal neoformans
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most commonly presents as meningitis** (low grade fever*, HA*, decreased cognitive function*, minimum nuchal rigidity & seizures may occur)
pulmonary disease is also possible: cough, fever, SOB, chest pn, etc. |
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diagnosis 101 of cryptococcal neoformans
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CSF culture**, clinical symptoms, elevated CSF opening pressure (stick needle in pts back)
india ink stain** |
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why is it VERY important to treat cryptococcal meningitis?
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it has a HIGH mortality rate!
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treatment regimen for cryptococcal meningitis
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Induction: Amphotericin B x 14d
(Flucystosine speeds clearance of yeast and helps prevent relapse; no initial improvement in mortality noted) Consolidation: fluconazole 400mg/day x 8 weeks or until CSF sterile Suppressive/maintenance: fluconazole 200mg/day (Continue until immune reconstitution occurs with HAART) |
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is prophylaxis warranted for cryptococcal meningitis?
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Primary: NOT routinely recommended
If done, use 100-200mg fluconazole at CD4<50 Secondary: Lifelong UNTIL immune reconstitution May stop with CD4≥100-200 for 6+ months, completed treatment course, and asymptomatic |
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this disease is caused by an organism that: Present in soil and water , domestic and farm animals, birds, foods, and some tobacco products – *we are exposed to it all the time*
Organism gains access through the gut or lungs, then spreads hematogenously |
Mycobacterium avium complex
comprised of M. avium, M. intracellulare (MAI) |
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what organs are involved and what are the s/sx of MAC?
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multiple organ involvement
s/sx - Non-specific for the most part Weight loss, intermittent fevers, chills, night sweats, abdominal pain, diarrhea, weakness, anemia No pulmonary symptoms* CD4 <50 = more common than you might think MAC = more of a dissmenated bug tuberculosis = pulmonary dysfunction respiratory failure MAC = likes to get into other places in body; bone marrow, GI tract, major organs i.e. liver severe anemia, severe GI distress (diarrhea, wasting) Most get a bone marrow biopsy – most common diagnosis w/MAC |
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therapy for MAC preferred regimens:
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Clarithromycin PO + ethambutol PO
Azithromycin IV/PO + ethambutol PO |
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therapy for severe MAC:
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Use one of the preferred regimens + one of the following: (3 drugs)
Rifabutin (3rd agent), quinolone antibiotic, or amikacin |
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primary MAC prophylaxis: when, how?
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*Primary*:
Start with CD4<50 D/C if CD4≥100 x 3+ months Agents: Azithromycin 1200mg qwk, clarithromycin 500mg bid, or rifabutin 300mg day Azithromycin easiest, safest, and most widely used Clarithromycin and rifabutin possess incr toxicity and drug interaction potential |
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secondary MAC prophylaxis: when, how?
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Secondary:
May stop if patient’s CD4≥100 for 6+ months, has completed at least 12 months of maintenance therapy, and asymptomatic. Agents: Macrolide (azitho/clarithro) + ethambutol ± rifabutin |
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MAC diagnosis:
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blood culture, bone marrow biopsy, stool culture
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