usmleasr
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HI EVERYBODY,
we will start discussion of AIDS -HIV now..about this discussion...everyone who views this forum must contribute to this topic(that is views=posts  )..read AIDS for a sec and add two points to this..
this forum is not complete until we finish discussing all about AIDS...
1.HIV STRUCTURE
2.PATHOPHYSIOLOGY OF INFECTION
3.various stages.
4.Oppurtunistic infections
5.treatment of oppurtunitic infections
6.HAART
7.HIV vaccines
even if i have missed any topic you have to add that..it is a collective notes for us to revise..so i want everyone to contribute ...becos we know these forums are very helpful to all of us ..
we start now friends...
HIV is human immuno deficiency virus..is a retro virus..
diploid RNA virus..with reverse transcriptase in it (RNA TO DNA)
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| mjl1717
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Some opportunists are Candida,Cryptospridium,T.B.Pneumocystis Carina Pneumonia, Mycobacterium Avium Intracellularae
Brief Description in the same order-psuedohyphae,cysts in diarrhea, acid fast +productive cough, ground glass appearance with methenamine silver stain,acid fast.
usmleasr -that is an excellent thought and is a great way to attack this ever changing scourge on mankind.
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| usmleasr
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thanks mjl..
HIV virus attacks mainly CD-4 cells...receptors for the virus on our cell are CD-4 AND CCR-5 :wink:
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| usmleasr
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Topics: 105
Posts: 970
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also about oppurtunistic infections..as cell mediated immunity is impaired first...infections are caused by..
1. intracellular bacteria
2.fungi
3.viruses
4.protozoa..
tackling of extracellular bacteria is normal for loooong time :wink:
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| mjl1717
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The first drug AZT decreased maternal transmission some reports say by 30%- 1)inhibits viral reverse transcriptase (RNA directed DNA polymerase)
There are newer agents which I will get to later.(today)
usmleasr-even if its only me and you we 'll cover it to the nth degree. Ill try to keep it to short distinct paragraphs or sentences,instead of 9 page articles. Ill get back with you :idea:
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| usmleasr
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thanks mjl for constant support
we will definitely cover...
now about viral genome..
env = for envelope proteins..GP-120; GP-41
gag = for nucleo capsid proteins, p24,p40;p55 etc
pol = for enzyme proteins ..reverse transcriptase,,protease...integrase etc
also it is high rate of mutation in HIV genome that allows its eternity after infection
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| asmi
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Regrading treatment :
:arrow: HAART( highly active antiretroviral therapy) ....i.e combination of 2 NRTI's and 1 Protease inhibitor(PI).....proved useful to decrease viral RNA, reverse the decline in CD 4 cells and decrease opportunistic infections.
:arrow: 2 NRTI'S + 1 PI ... namely ZDV( zidovudine) ,DDI( didanosine) and PI( indinavir/ritonavir/ saquinavair)
:arrow: There are NNRTI's too...namely nevaripine , efavirenz ,which are not myelosuppressive .Therefore the event of Protease sparing combination ( ZDV+DDI+ NIVARIPINE)
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| asmi
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:arrow: NNRTI's don't need to get phosphorylated and they r not incorporated into viral DNA ...they bind directly and noncompetitively to reverse transcriptase .
:arrow: Needle stick injury: ZDV+ 3TC..1 month or ZDV+3TC+ INDINAVIR for 4 weeks .
:arrow: in pregnancy: ZDV full dose , in tirmester 2 and 3 + 6 weeks to baby.
adverse effects :
:arrow: ZDV.... : hematotoxicity
:arrow: DDI...pancreatitis
:arrow: D4T,DDC.....peripheral neuropathy
:arrow: lamuvidine...GI effects/neutropenia...can be used in HBV also.
:arrow: PI's : indinavir..nephrolithiasis
* all PI's can cause central obesity and insulin resistance( disordered lipid and CHO metabolism)
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| crista
Forum Guru
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mechanisms for evadind the immune sist:
-integration of viral DNA in dna of host;
-mutation of env gene
-tat and nef prot. that down regulate mhc1.
mutation in nef and tat :arrow: increased patogenity????????????????
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| usmleasr
Forum Guru
Topics: 105
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hi asmi ..thanks for joining us...in this
now coming to CD-4, CCR-5 receptors..
CD-4 binds to gp-120 of virus..but a co-receptor called chemokine recptor CCR-5 is also needed....that's why few people are resistant to HIV infection due to mutation in this receptor...but CMV infection can promote HIV infection becos it codes for a receptor very similar to CCR-5 ..interesting isn't it? :wink:
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| asmi
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thanks usmleasr,
:arrow: highest mutation rate seen in pol gene . Nef gene tends to keep infection in latent state. Vif gene is rquired for infectivity. Tat gene is potent promotor of viral activity .
:arrow: therefore vaccines are aimed at the above genes and env gene.
:arrow: LAB DIAGNOSIS:
1. ELISA..detects antibodies (in pt's serum )to antigens P24 ,P17 ,gp 120,gp 41. ANTI-P24 is first antibody to rise but goes early where as env antibodies rise slowly but last longer .
2. western blot ...
:idea: first ELISA...IF positive then repeat it ( second time)..if positive then go for western blot test .
3. PCR...HIV DNA PCR done to detect viral load
4.capture p24 antigen in culture...for newborns whose mom's are HIV+ and also for assessing drug resistance .
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| usmleasr
Forum Guru
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PCP pneumonia
fever +dyspnoea+nonproductive cough
DX- by CXR showing typical perihilar infiltrates
BAL showing foamy exudate
microscopy with gomari methinamine silver stain showing boat shaped or crushed ball like org
giemsa and immunoperoxidase stain also can be used
treatment...high dose SMX-TMP
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| crista
Forum Guru
Topics: 121
Posts: 408
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meningitits-most common:cryptoccocus
CSF-ink dye-capsule
treatment:amfotericin B+ flucytosine
profilaxy:fluconazole
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| anne
Forum Elite
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visual compromise in AIDS pt---CMV retinitis,or brain mass of toxoplasmosis or lymphoma.
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| crista
Forum Guru
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cmv retinitis-gancyclovir
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| asmi
Forum Hero
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:idea: acid fast cyst in stools...cryptosporidum
:idea: cysts in stool ......isospora belli
:idea: SOL/ring enhancing lesions on MRI( in brain.)...toxoplasma gondi
:idea: CMV... Owl's eye (basophilic intranuclear inculsion bodies)
:idea: PML...also seen in HIv+ pts
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| crista
Forum Guru
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PML is a lethal secondary viral infection mostly occurring in AIDS patients with advanced immunodeficiency. The JC virus is a ubiquitous virus, able to enter the brain and lytically infect oligodendrocytes
Symptoms including weakness, loss of sensation, visual loss, changes in balance and coordination. Because it is usually relentlessly progressive, severe neurologic disability develops over a period of 2-6 months with death following rapidly from general disability.
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| usmleasr
Forum Guru
Topics: 105
Posts: 970
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mycobacteria infections
Multi drug resistant tuberculosis is common in AIDS..
atypical mycobacteria target cells of MPS(liver, spleen, bone marrow ) :icon_thumb:
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| galleta
Forum Newbie
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Posts: 9
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:!: HIV infection lacks a phase of true latency.
:!: Common Neoplasms - Kaposi, B cell non-Hodgkin lymphomas, Primary lymphoma of te brain and invasive cancer of cervix
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| jayesh
Forum Junior
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people with hiv + can be grouped into 3 categories
category A pt having acute symptoms ( fever, malaise, persistent gen lymphadenopathy) or assymptomatic
A1 CD4+ > 500
A2 CD4+ 200-499
A3 CD4+ <200
category B syptomatic pt (constitutional sym fever > 38.5C, diarrhoea> 1mth, leucoplakia, candidiasis)
B1 B2 & B3 based on CD4+ count as above
category C ADC (all opportunistic ds, bacteria, fungi, virus, parasites, cancers)
C1, C2 & C3 based on CD4+ count as above
AIDS = persons in category A3 or B3 or C1-3
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| galleta
Forum Newbie
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Various stages: :arrow: 1) Acute/Early phase: 50-70% pts have self-limited acute illness (fever, myalgias, weight loss, cervical adenopathy). High level of viral production and widespread seeding of hte lymphoid tissue. :arrow: 2) Middle/Chronic phase: Relative containment of the virus. Pts either asymptomatic or develop persistent generalized lymphadenopathy. :arrow: 3) Final/Crisis phase: Breakdown of host defense, dramatic increase in plasma virus with AIDS defining diseases. CD4+ count below 500.
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| anne
Forum Elite
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infections in AIDS pts which cant occur in any other condition:
PCP
candida esophagitis
kaposi sarcoma
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| mjl1717
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Genital ulcerations from T.Palladium, Haemophilus ducreyi , and Herpes simplex increase susceptibility to infection and infectivity. (Either way if you test for HIV its good medicine to test for All common STD's)
The rate of transmission of HIV from untreated mother to to infant is 25% in the U.S.
Although HIV can be isolated from saliva, this has occured in only a small percentage of infected individuals. Furthermore, a proteincontained in saliva called "secretory leukocyte protease inhibitor", has been shown to possess anti- HIV-1 activity in vivo.
Leading cause of death 25 to 44 years of age in the U.S.
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| mjl1717
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upregulate HIV --herpes simplex ,CMV,human herpes virus 6, EpsteinBarr
HepatitisB, adenovirus, psuedorabies virus, HTLV1,
Mycoplasma induces HIV expression!
Active tuberculosis ACCELERATES HIV!
Those were only the exogenous upregulaters!
The main endogenous upregulaters are CYTOKINES! IL1 IL2 IL3 IL6 IL12
both TNFs, (M-CSF), the most potent are the "proinflammatory cytokines"
TNF alpha,IL1B, and IL6. Interferon alpha and interferon beta suppres HIV
replication whereas (TGF-B), IL4, IL10, and IFN-gamma can either suppress or induce HIV infection depending on the system involved!
:idea:
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| usmle prep
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high risk population fot HIV:
HOMOSEXUAL MEN 75%
intravenous drug abusers 15%
hetero sexual partners of persons with high risk group 4%
pt.receiving multiple blood transfusions 2%
haemophiliacs 1%
infants of high risk parents
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