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248 Cards in this Set

  • Front
  • Back
which region has the largest prevalence of AIDS?
Sub-Saharan Africa
who are most new cases of AIDS in the US? (2)
who constitutes the largest transmission category in the US?
what is the tansmission rate among the uninfected vs the infected?
7% vs 2%
what is the only dsRNA virus?
reovirus, specifically rotavirus
what makes HIV a unique retrovirus?
it has 2 copies of ssRNA
what is gp120? (2)
a surface glycoprotein
the first molecule that attaches to the host cell
how does gp120 avoid being detected?
heavy glycosylation
what does gp120 bind to? (2)
CD4 and CCR5
what is gp41? (2)
a transmembrane protein
most important molecule for viral entry
what is matrix protein 17?
helps to maintain the viral structure and transport the viral genome to the host cell nucleus and assemble new virions
what is p24? (2)
a caspid protein
the first antigen the body will make an antibody to, therefore the p24 antibody is the best way to detect the presence of HIV in ELISA
what are the 3 critical enzymes for HIV?
reverse transcriptase
where is HIV-2 seen? (2)
west africa and india
how is hiv-2 different?
progression to AIDS is slower
what does gag code for? (3)
matrix, caspid, and nucleocaspid
if gag is mutated, what might we see?
drug resistance to drugs targeting p24
what does pol code for? (3)
the critical proteins
reverse transcriptase
if pol is mutated, what might we see?
resistance to protease inhibitors
what does env code for? (2)
what does tat code for?
positive regulator of transcription
what does rev code for?
regulator of viral expression
what is the regulator of viral expression?
transfers spliced and unspliced molecules from the nucleus to the cytoplasm
what does nef code for?
negative regulation factor
why is nef important?
the negative regulation factor is essential for the progression to AIDS
what does nef do? (2)
augments viral replication in vivo and in vitro
down-regulates CD4 and MHC class II
why might someone be infected with HIV for 15 years and not progressing to AIDS?
a mutation in the nef protein
what type of mutation do non-caucasions usually have?
what type of mutation doe caucasions ususally have?
what will macrophage-trophic viruses express?
CCR5 receptor
what will lymphocyte-trophic viruses express?
why are macrophages the 1st cells to be infected?
because of their strategic location at the mucosal surface
what is viral penetration mediated by?
fusion of viral gp41 with the host cell plasma membrane
what type of genetic material is synthesized and by what?
DNA copy synthesized by RNA dependent DNA polymerase
what does integrase do in HIV?
circularizes DNA and incorporates it into the host cell genome
when the host cell is activated, what happens? (3)
viral DNA is transcribed yielding messenger RNAs and viral genome RNA
what will NF-kappa-B do in HIV?
transcibes and translates Tat and Rev
what are tat and rev?
RNA proteins in HIV
what does Rev do in HIV?
regulates the number of RNA that will be transferred from the nucleus to the cytoplasm
what does tat do in HIV?
amplifies transription of viral RNA
what are the late proteins in HIV (3)?
gag, pol, env
what happens to the late proteins in HIV?
they are cleaved and assembled with genomic RNA into virions which bud from the cells
why do host cells lyse in HIV?
at some point the cell gets exhausted and dies after some time
what do NK cells mediate in HIV?
attack of HIV specific cytotoxic T cells
what does ADCC do in HIV?
kills antibody identified cells
what do B cells do in HIV?
not directly damaged, but in order for the B cells to be functional they need help from the Th2 cells which are also under attack so they become useless
what is Acute retroviral syndrome and how does it manifest?
the fist sign of HIV, in which the patient suffers from flu-like symptoms and is usually considered to be a cold or flu
what is the symptomatic stage of HIV? (2)
opportunistic infection or malignancies
what are 4 opportunistic infections in HIV?
what are 4 malignancies in HIV?
kaposi sarcoma
burkitt's lymphoma
cervical carcinoma
anal carcinoma
burkitt lymphoma
what may lead people to be a long-term non-progressor?
a NEF or CCR5 mutation
how is viral load expressed?
in mL
how is CD4 cell count expressed?
in microL or mm^3
what is the CDC definition of AIDS? (2)
patient has to be HIV+ and CD4 count below 200
patients who are HIV+ with a total T cell count less than 14%
What are 4 differential diagnosis possibilities of AIDS?
secondary syphillis
acute early hep B or A
how do you know if a patient has a CMV form of mono?
the heterophile test will be negative
what is diagnostic method 1 for AIDS?
symptoms are consistent with acute retroviral syndrome
negative HIV ELISA within past 6 months
positive HIV ELISA at current testing
what is diagnostic method 2 for AIDS?
symptoms are consistent with acute retroviral syndrome
negative HIV ELISA at current testing
High HIV RNA titer at current testing
Is PCR qualitative or quantitative?
is RT-PCR qualitative or quantitative?
what type of diagnostic method would you use for a baby born to a mother with HIV and why?
you already know the baby will have the antibodies, you want to know if the baby has the viral RNA
what type of diagnostic method would you use for a patient you are treating and want to know if they have gotten better or not?
why does ELISA have to be confirmed with western blot?
because ELISA is a highly sensitive test so it can give false positives
if viral serology is negative, what might the differential diagnosis include? (5)
idiopathic CD4+ lymphocytopenia
Sjogren syndrome
congenital immunodeficiency syndromes
how can vertical transmittion be avoided? (5)
elective c section
28 weeks onward go on AZT
given NRTI inhibitor at delivery
babes given anti-retrovirals for a week
no breast feeding
how do you treat post-exposure prophylaxis?
give at least 2 drugs for 2-3 months
what is the initial immune response to HIV? (3)
antibodies to the envelope protein
antibodies to the cytotoxic T cells
antibodies to the HIV core protein
how does the body lose ground against HIV?
when the envelope protein changes, the antibodies against it become useless; as the antibodies adjust, the virus has time to change even further
why do viruses have so many mutations?
because they do not have a good proof reading system
what are 4 ways HIV evades the immune system?
rapid multiplication
high mutation rate (antigenic variation)
elimination of CD4 T cells
misdirected and exhausted B cell response
how does strep pneumonia avoid the immune system?
uses a capsule to avoid phagocytosis
how does mycobacterium tb avoid the immune system?
by blocking lysosome fusion with the phagosome it avoids antibody and complement opsonization
how does listeria monocytogenes avoid the immune system?
it escapes the phagosome
what is an important side effect of INH + Pyridoxine?
strong peripheral neuropathy
what does HAART do?
does not cure but controls retroviral replication
when is the HAART goal achieved?
when the plasma viremia level drops below detectable levels (50mL or less)
what is the recommended agent for TB prophylaxis?
INH + pyridoxine
according to the books, when should HAART begin? (2)
Any patient with symptoms of when CD4 count falls below 200
in practice, when should HAART begin?
when CD4 hits 350
what is ATRIPLA?
a combination of 3 HIV medicines
efavirenz (sustiva)
emtricitabine (emtriva)
tenoforvir (viread)
what is the MOA of NRTIs?
structurally similar to purine and pyrimidine components of the viral nucleic acid
NRTIs get incorporated into the growing DNA chain and block the completion of the DNA strand
what type of drug is zidovudin (azt)?
what type of drug is stavudin (D4T)?
what type of drug is larnivudin (3TC)?
what type of drug is didanosine (ddI)?
what type of drug is zalcitabine (ddC)?
what type of drug is nevirapine?
what type of drug is delavirdine?
what type of drug is efavirenz?
what type of drug is saquinavir?
protease inhibitor
what type of drug is ritonavir?
protease inhibitor
what type of drug is indinavir?
protease inhibitor
what type of drug is nelfinavir?
protease inhibotor
how do protease inhibitors work?
prevent packaging of viral proteins in the virion
how does the herpes virus evade the immune system?
persists in the host cells without dividing to avoid the immune system recognition
how does strep pneumonia, influenza virus, and HIV avoid the immune system?
use antigenic variation to avoid memory response
how does neisseria, strep pneumonia, and haemophilis influenza avoid the immune system?
expresses IgA protease to avoid IgA neutralization
how does EBV avoid the immune system?
inhibits host cell expression of LFA-3, ICAM-1 to block adhesion of CTL to infected cells
how do herpes simplex and CMV avoid the immune system?
inhibits host cell class I expression to block CTL recognition
how does mycobacterium leprae avoid the immune system?
stimulates Th2 response to suppress Th1 response
what type of vaccine is contraindicated in AIDS?
live vaccines
what is a major consideration in immunizing AIDS pts?
is T cell numbers are low, will the patient even be able to benefit from an immunization?
is the pneumococcal vaccine advised in AIDS?
yes, every 5 years
is the influenza vaccine advised in AIDS?
yes, the inactivated vaccine annually
is the hepatitis B vaccine advised in AIDS?
yes, 3 injection sites if not immune
if the hepatitis A vaccine advised in AIDS?
yes, with a 2 injection series with underlying liver disease and no immunity
is the tetanus-diptheria vaccine advised in AIDS?
yes, every 10 years
is MMR advised in AIDS?
not if CD4 is less than 200, otherwise per routine
is oral poluomyelitis vaccine advised in AIDS?
is the oral typhoid vaccine advised in AIDS?
is the BCG vaccine advised in AIDS?
is the varicella-zoster advised in AIDS?
no, use herd immunity
is the yellow-fever vaccine advised in AIDS?
when do you begin prophylaxis for pneumocystis jiroveci in AIDS?
when CD4<200
what do you use for prophylaxis for pneumocystis jiroveci in AIDS?
when do you begin prophylaxis for mycobacterium avium complex in AIDS?
when CD4<50
when do you begin prophylaxis for toxoplasmosis in AIDS?
when CD4<100 and positive anti-toxo IgG assay
when do you begin prophylaxis for tb in AIDS?
with induration >5mm
what do you use for prophylaxis for mycobacterium avium complex in AIDS? (3)
what do you use for prophylaxis for toxoplasmosis in AIDS?
what are 2 second line AIDS drugs?
fusion inhibitors
integrase inhibitors
how do fusion inhibitors work?
inhibit gp41 from fusing with the host membrane
what is an example of a fusion inhibitor?
enfuviritide (fuzeon)
what is an example of an integrase inhibitor?
raltegravir (isentress)
what 2nd line AIDS drug must be given in combination with other drugs?
integrase inhibitors
how does integrase inhibitor work?
inhibits the integrase protein from HIV DNA from meshing with healthy cell DNA
what is merovoc?
CCR5 antagonist
what is the problem with waiting until the CD4 count drops to admin HAART?
once the CD4 drops other manifestations of AIDS begin to develop (i.e. opportunistic infections) that you must treat as well
why should you never use a protease inhibitor by itself?
single use leads to selection of the resistant strains resulting in progression to AIDS whereas RTIs require 3 or 4 independent mutations
what is a thyroid complication associated with HAART?
elevated TSH with normal T3 and T4 (normally T3 and T4 would go down)
what 2 HAART drugs is an elevated bilirubin associated with?
what 4 hematological complications are associated with AZT?
what are 5 ways a retrovirus can transform a cell into a malignant one?
utilizing the cell machinery for a long period of time which transforms it into a malignant cell
integrating into the host cell genome
insertional mutagenesis (activating a proto-oncogene)
expression of transgenes
frame shift mutations
what are transgenes?
new genes that activate trancription factors in the cell which activate proliferation
what do you need for kaposi sarcoma?
co-infection of HIV and HHV-8
what virus in addition to HIV causes kaposi sarcoma?
what will a kaposi sarcoma look like and what will its color depend on?
amber red or deep purple
color depends on whether it is an artery or vein that is affected
in kaposi sarcoma, what induces prolioferation of endothelial cells?
VEGF, induced by tat
what can kaposi sarcoma tumor be confused for?
basillary angiomatosis
how can you differentiate between basillary angiomatosis and kaposi sarcoma?
basillary angiomatosis is caused by bartonella henslease which is associated with cats
what favors the malignant transformation of kaposi sarcoma cells?
what 2 things will you see in later tumor formations of kaposi sarcoma?
spindle shaped cells
where is burkitt lymphoma prevalent?
west africa
if something looks like burkitt lymphoma but is in asia, what is it?
nasopharyngeal carcinoma
how does EBV gain access to the b cell in burkitt lymphoma?
via CD21 which is the EBV receptor on the b cell
how are latent B cells activated?
what 2 HPV types will cause cervical and anal carcinoma?
16 and 18
when does HPV replication increase?
when host cellular immunity decreases
what 2 things does HPV do to cellular replication?
induces cellular replication while simultaneously disregulating replication
how often should HIV+ individuals be screened for precancerous conditions in the cervix or anus?
what 2 things will you look for in a pelvic exam for cervical and anal carcinomas?
cervical intraepithelial neoplasia
what are koilocytes?
abnormal cell with a large nucleus surrounded by a perinuclear halo
when should you begin prophylaxis for CMV?
when should you begin prophylaxis for cryptococcus?
what causes progressive multifocal encephalopathy and will appear as white sclerotic plaques?
JC virus in HIV
how will JC virus in HIV present?
progressive multifocal encephalopathy and will appear as white sclerotic plaques
why is toxo a commonly encountered problem in HIV?
because 50% of the US population is seropositive for toxo
what is the invasive form of toxo?
what is the infective form of toxo?
what is the number 1 source of toxo?
undercooked pork
where does toxo undergo sexual and asexual development?
in the GI tract of the cat
how is toxo excreted from the cat?
as an immature oocyst
when do problems arise for humans with toxo infections?
when it gets into circulation and can enter the brain
what are 3 problems seen if a baby is exposed to toxo early in utero?
CNS problems
how is toxo presented when the baby is exposed later on in utero?
won't present until the 2nd or 3rd decade of life
blindness (chorioretinitis)
how will immunocompetent adults present with toxo infection?
similar to mono
how will immunocompromised present with toxo infection? (4)
encephalopathy which will present as
diffuse encephalopathy
mass lesion
what is the definitive sign of toxo?
ring enhancing lesion in the brain
what percent of AIDS patients will get toxo?
of those AIDS patients exposed to toxo, what percent will die?
how is toxo treated?
sulfonamide + pyrimethamine
how is toxo treated in pregnant women?
replace pyrimethanine with spiromycin
what toxo treatment is effective against both encysted and trophozoite forms?
what parasite will cause intractable diarrhea?
crytosporidium gastroenteritis
how can you ID cryptosporidium cysts?
they will be acid-fast positive
what is the morphology of cryptosporidium?
spherical structures arranged in rows along the microvilli of epithelial cells
what are 3 other AFB parasites that cause diarrhea?
where does crytosporidium go through sexual differentiation?
in human intestines
what form of crytosporidium are males?
what form of cryptosporidium are females?
which form of cryptosporidium can auto-infect?
thin walled oocyst
which form of cryptosporidium can infect outside the body?
thick walled oocyst
why doesn't cryptosporidium need a second host?
becuase both sexual and asexual life cycles occur in humans
how does cryptosporidium cause intractible diarrhea?
affects the jejunum to prevent absorption which leads to deficiencies
leads to atrophied villi with widened crypts
how do you treat cryptosporidium?
only way is to improve CD4 count; there is no cure
what is the most common site of infection for mycobacterium avium complex?
how will you know a patient has mycobacterium avium complex and not TB?
TB screening will be negative
TB will not have diarrhea
how will you treat mycobacterium avium complex?
azithromycin or other macrolide
what is the main mainfestation of mycobacterium avium complex? (2)
cavitary pulmonary lesion that has disseminated
how do you diagnose mycobacterium avium complex?
blood culture
how is mycobacterium kansasii similar to TB? (2)
symptoms will be similar
PPD positive
how will you treat mycobacterium kansasii?
traditional TB drugs
how will you differentiate mycobacterium kansasii from TB?
mycobacterium kansasii is unique because it is photochromogenic (produces a pigmented colony in the presence of light)
how is pneumocystis carinii a unique fungus and what 2 implications does this have?
does not have ergasterol on cell membrane
therefore we cannot treat it with a traditional antifungal
harder to stain
how will pneumocystis carinii stain?
with silver stain
what is the epidemiology of pneumocystis carinii?
ubiquitous (we've already developed an infection)
where will pneumocystis carinii epidemics be found? (3)
hospitalized infants
elderly nursing home residents
malnourished infants
what type of response will immunocompetent individuals develop to pneumocystis carinii? (2)
cell mediated
humoral response
where do pneumocystis carinii spores attach and what implication does this have?
spores attach to the alveolar walls so sputum samples will be useless
what is a long lasting effect of pneumocystis carinii?
the alveolar walls become thickened and scarred, preventing the free passage of oxygen
what are 3 symptoms of pneumocystis carinii?
non-productive cough
what does pneumocystis carinii require for diagnosis?
requires a living creature
what will you see on a CXR for pneumocystis carinii?
interstitial pneumonia
linear opacities with hazy ground glass appearance
what type of sample should you use for pneumocystis carinii diagnosis? (2)
BAL or biopsy
what type of stain can you use for pneumocystis carinii with BAL?
what type of stain can you use for pneumocystis carinii with biopsy? (2)
methenamine stain
silver stain
how will pneumocystis carinii appear on biopsy?
honeycomb appearance
what is cryptococcus neoformans?
a unique fungus that is a respirator pathogen but will present with menigneal encephalitis
what is an important virulence factor in cryptococcus neoformans?
polysaccharide capsule (GXM)
why is it problematic that cryptococcus neoformans is thymus independant?
it does not require T cells to develop an immune response so no memory will be developed because you need T cells to induce class switching in B cells; you'll only get IgM which cannot induce a memory response
how will cryptococcus neoformans grow? (3)
at body temperature
on a variety of media
colony morphology resembles bacteria
what type of stain will show the thick capsule of cryptococcus neoformans?
indian ink
where will cryptococcus neoformans be found?
soil contaminated with pigeon droppings
when does cryptococcus neoformans begin replicating?
as soon as it enters the blood stream
what does cryptococcus neoformans produce that allows it to replicate inside the macrophage?
melanin which prevents oxidative injury
if cryptococcus neoformans encysts in the brain, how will it present?
loss of consciousness (key symptom)
what is the latex agglutination test?
looks for the antigen rather than the antibody
what can latex agglutination test be used for? (4)
strep pneumonia
haemophilis influenza
neisseria meningitis
cryptococcus neoformans
how is cryptococcus neoformans treated? (3)
amphotecerin B in combination with flucytosine or fluconazole
what percent of cryptococcus neoformans patients suffer from residual damage?
what is the number one cause of in-utero infections in the US?
how does CMV become latent?
uses the mononuclear cell
what is the key morphological feature of CMV?
basophilic internuclear inclusion body with a large halo
what percent of adults are sero positive for CMV?
how is CMV transmitted?
close personal contact
sexual contact
organ transplant
vertical transmission
what does CMV infect?
what does CMV do in an infected cell?
remains in a non-replicating and non-infectious form
what is the difference between CMV iinfection in monocytes vs lymphocytes?
monocytes - replication is very slow
lymphocytes - cell becomes quiescent
who are susceptible to reactivation in CMV?
organ transplants
what is a blueberry muffin baby (3) and what is it associated with?
associated with CMV
thrombocytopenic purpora
yellow and red will turn blue
how does CMV present? (4)
blueberry muffin baby
what will acute CMV infections present like?
in what population is CMV pneumonia the #1 cause of pneumonia?
bone marrow transplant
what is the key feature of CMV?
how do you prevent CMV?
anti-CMV globulin
what 3 drugs are used for CMV treatment?
what is the MOA of gancyclovir?
inhibits DNA polymerase
what is a side effect of gancyclovir?
bone marrow suppression
what is most effective in decreasing the mortality of CMV pneumonia?
combination of gancyclovir and immuno-globulins
what is the MOA of foscarnet?
inhibits DNA polymerase
what is a side effect of foscarnet?
what is cidofovir used for?
what three things indicate the presence of HIV? How many must be present to make an official diagnosis?
must have 2/3
what is the normal ratio of CD4:CD8?
what happens to the CD4:CD8 ratio in AIDS?
reverses; becomes 1:2
what are two physical findings of meningitis?
kernig's sign
If a patient was seropositive for toxo and then became infected, which immunoglobulin will increase?
If a patient was seronegative for toxo and then became infected, which immunoglobulin will increase?