AIDS pathology – Flashcards
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| what is common target for HIV? |
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| the lymph nodes where changes occur to T cells, some malignant/some benign |
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| what is a lymphoma? |
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| a malignant neoplasm visible in lymphoid tissue (nodes) or extra-nodular lesions (GI tract, brain) |
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| how does the process of HIV-related lymph node pathology start? what is the manifestation of this? |
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| T cells are infected by HIV leading to lymph node enlargement/follicular hyperplasia, which is seen clinically as lymphadenopathy (often bilateral, can be either painless (usually neoplasm associated) or painful (usually due to an infection) |
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| how do germinal centers behave in lymph nodes of AIDs pts? does this affect B cells? |
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| the germinal centers of lymph nodes usually merge with the interfollicular area (change in microscopic architecture of the lymph node), usually effecting the B cell areas of the node |
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| are B cells activated by HIV action in lymph nodes? |
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| yes, and this causes hypergammaglobulinema |
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| as AIDs progresses, what happens to the follicles? |
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| the follicles involute and break down, disrupting the organized network of dendritic cells |
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| as AIDs progresses, what happens to the germinal centers? |
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| the germinal centers are hyalinized/scarred |
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| what is persistent generalized lymphadenopathy (PGL)? is there a differential diagnosis for PGL? how is it diagnosed? |
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| 2 or more non-inguinal sites (cervical, submandibular, occipital, axillary, epitrochlear) expressing non-tender follicular hyperplasia. retroperionteal, mesenteric, and mediastinal involvement is seen, hilar is NOT typical. differentials include neoplastic changes, lymphomas (hodgkin's/non-hodgkins), TB, and castleman's disease HHV-8. diagnosis consists of a needle bx or sx incision |
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| what might be seen on a salivary gland bx? |
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| epithelial hyperplasia and lymphocytic infiltration -> seen often |
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| do AIDS pts develop lymphoma? what is the main predisposing factor? what types are there? |
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| 6% of AIDS pts develop lymphoma, for which immunodeficiency is the main predisposing factor. AIDS lymphomas can present differently and are divided according to location: systemic, CNS (brain lymphoma should make you think HIV), body cavity lymphomas |
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| how do AIDS lymphomas form? are other viruses implicated in their formation? |
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| AIDS lymphomas are the result of polyclonal B cell activation followed by monoclonal/oligoclonal B cell population, stimulated by viruses like EBV which are able to proliferate b/c of HIV infection. HIV doesn't directly cause lymphomas, but allows them to form. the EBV genome is seen in many AIDS lymphomas and is likely the cause of the high level of cytokines, IL-6 and growth factors -> neoplastic B cells will have many neoplastic clone B cells eventually leading to cancer |
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| what kind of lymphoma is seen more often with AIDS pts? where in the body are they commonly seen? |
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| non-hodgkin's which is 75-80% systemic, 20% CNS (immunoblastic), and 5% primary effusion lymphoma |
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| what is the histology of AIDS NHLs? |
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| AIDS non-hodgkins lymphomas are 40% large cells and immunoblastic and 40% are burkitt/burkitt-like |
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| how has HAART affected the median time between HIV and NHL diagnoses? NHL survival time from diagnosis? |
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| the median time as tripled, and the median survival time has doubled |
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| what is the mechanism of EBV-induced non-hodgkins lymphoma? |
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| the EBV latent membrane protein-1 (LMP-1) protects B cells from apoptosis by inhibition of BAX (apoptotic) and upregulation of BCL2 (anti-apoptotic). LMP-1 also contains 2 C-terminal activation regions which bind to the TNF associated receptors w/activation of the NFkB signaling pathway |
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| what are some characteristics consistent with malignancy in lymphocytes? |
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| prominent nucleoli, prominent nuclear membrane and large size |
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| what are angiocentric lymphocytes? |
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| blood vessels with various neoplastic lymphocytes surrounding them, they are associated with EBV |
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| if an HIV patient presents with mental status changes, seizure activity, what should be in the differential? |
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| lymphoma |
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| what are HIV related factors that lead to the decline in CD4+ lymphocyte level? |
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| apoptosis of infected cells (cytopathic effect), CD8+ attack, colonization of GALT, spleen, loss of CD4+ T cell progenitor stem cells, syncytial fusion, apoptosis of uninfected CD4+ cells (via binding of gp 120 to the receptor) |
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| what is seen pathologically the first stage of HIV? |
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| asymptomatic, persistent generalized lymphadenopathy |
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| what is seen pathologically the second stage of HIV? |
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| weight loss, predisposed to infections such as HSV, HPV, VZV, neoplasms |
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| what is seen pathologically the third stage of HIV? |
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| candidiasis, dysphasia, difficulty swallowing, hairy leukoplakia, pts possibly bedridden |
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| what is seen pathologically the fourth stage of HIV? |
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| defining opportunistic infections, pneumocystis carinii, neoplasms, kaposis sarcoma (HHV 8), bedridden |
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| what are some skin & oral lesions seen w/HIV? |
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| hairy leukoplakia, candida albicans, gingivitis, periodontitis, HSV 1&2, molluscum contagiosum, bacillary angiomatosis (bartonella henslae), kaposi's sarcoma (vascular sarcoma, HHV-8) |
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| what can herpes zoster follow on pt's bodies? |
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| dermatones, L5 is a common presentation |
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| what are base-line tests for HIV? |
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| CD4 count, plasma HIV-RNA, HIV genotype to determine ARV resistance |
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| why might a CBC be done for newly diagnosed HIV+ pts? |
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| anemia may contradict use of zidovudine |
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| why might a chem 12 (renal) test be done for newly diagnosed HIV+ pts? |
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| azotemia contraindicates used of tenofovir, high glucose prevents use of protease inhibitors (insulin resistance) |
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| why might a bilirubin, HCV test be done for newly diagnosed HIV+ pts? |
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| to make sure the liver can withstand ARV hepatoxicity |
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| why might a lipid profile be done for newly diagnosed HIV+ pts? |
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| to ensure protease inhibitors aren't contraindicated |
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| should comorbidities such as SCC (women), Hep B,C, CMV, toxoplasmosis, HPV be checked with new HIV+ pts? how |
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| yes, via serological testing |
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| has more TB been seen since HIV, is it tested for? |
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| yes and TB is tested for w/new HIV pts |
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| why would an EKG be ordered for a new HIV+ pt? |
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| to check on vascular effects of protease inhibitors |
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| what diseases can be seen at 500 CD4+ levels? |
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| kaposi's sarcoma, lymphoma, TB |
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| what diseases can be seen at 250 CD4+ levels? |
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| pneumonia jiroveci pneumonia, toxoplasmosis, brain, candidial esophagitis |
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| what diseases can be seen at 100 CD4+ levels? |
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| CMV, cryptoccosis, mycobacterium avium complex infection, microsporidiosis, HIV encephalopathy, progressive multifocal leukoencephalopathy |
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| what % of pts have some degree of CNS involvement at autopsy? how does it present? |
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| 90% CNS involvement may be the sole or initial presenting feature of HIV infection, examples include lymphomas, self limited meningoencephalitis, aseptic meningitis, vacuolar myelopathy, peripheral neuropathy, and AIDs dementia complex |
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| what are the organisms that cause toxoplasmosis and associated pathologies? |
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| t. gondii has 2 protozoal forms, tachyzoite (causes tissue injury), and bradyzoite (fills cysts/pseudocysts which collect around neurons/perivascular macrophages). toxoplasmosis leads to central necrotic masses surrounded by edema and inflammation. this is accompanied by perivascular infiltration, lymphoid infiltration, aggregates, endothelial swelling, thrombosis, fibrinoid necrosis, and fibrous obliteration of vessels = can lead to ischemia, organ death, seizure |
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| where is toxoplasmosis generalized? how does it present? |
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| toxoplasma gondii is often seen as a space-occupying lesion in the cerebral cortex, basal ganglia, brain stem (neuron rich areas) of AIDs pts and may appear as a tumor on an MRI. it presents as seizures, hemiparesis, cranial nerve deficits (should be picked up on in H&P), but some pts may only present with H/A, fever and lethargy |
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| what is seen on toxoplasmosis MRIs? |
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| ring enhancing lesions that mimic tumors |
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| what is the most common CNS mycosis? how does it present? |
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| cryptococcus neoformans, which presents in the brain as choroid plexus based masses (cryptococcomas), that often consist of gelatinous material due to capsular mucopolysaccharides |
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| is cryptococcus neoformans found in other organs than the brain? |
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| yes, but the brain is most common (either in brain or on meninges) |
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| what is progressive multifocal leukoencephalopathy? |
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| a demyelinating disease seen with defective cell mediated immunity, caused by some DNA viruses such as JC and HIV-1 |
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| what are symptoms of progressive multifocal leukoencephalopathy? |
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| motor deficits, cognitive decline, visual loss (pt may first present to opthamologist), gradual cognitive decline |
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| where is progressive multifocal leukoencephalopathy found? |
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| usually in the cerebral hemispheric white matter, usually attracted to oligodendrolions - causing enlargement of nuclei, dissolution of chromatin and replacement by basophilic "ground glass" material |
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| what is seen with progression of progressive multifocal leukoencephalopathy? |
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| progressive multifocal leukoencephalopathy develops into an expanding zone of oligodendroglial loss and infiltration of macrophages ingesting myelin. it appears as yellowish gray discoloration of white matter which may progress to white matter cavitation. florid astrogliosis with bizarre nuclei replace destroyed tissue (no scar tissue in brain) |
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| what kinds of trophic changes are seen with virally (JC/HIV-1) infected cells? |
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| inlusion bodies and multinucleated cells |
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| what is AIDS dementia complex associated with? who is it seen in? |
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| encephalitis w/multinucleated microglial cells, CD4 < 500. it is seen in 15% of HIV+ adults, but 30% of HIV + children. |
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| what are clinical symptoms of AIDS dementia complex? what can it mimic? what would be seen on an MRI? |
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| memory loss, impaired comprehension, apathy, tremor, gait disturbance, hyperreflexia, and apraxia - it can mimic other CNS disorders. an MRI would show diffuse or total cerebral atrophy, T2 white matter and hyper intensity |
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| what are some common AIDS-related carcinomas? |
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| aggressive SCC in uterine, anal areas. HPV prevalence is also high due to immunosuppression |
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| why might AIDS pts have more GI problems? |
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| some due to tx: protease inhibitors (nelfinavir, ritonavir), but also due to opportunisitic infections from CMV, cryptosporidium, c. dif, enterobacteriaceae, salmonella, mycobacterium avium complex (AIDS defining illness - aggressive TB form), and giardia |
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| what are some pulmonary manifestations of AIDS-related pathology? |
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| often opportunistic infections, pneumocystis carinii pneumonia, other pneumonias. lymphocytic interstitial pneumonitis and nonspecific interstitial pneumonitis. pulm. HTN is also seen |
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| how does pneumocystis jirovecii pneumonia present? |
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| cuplike cysts in the alveoli |
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| what is a common AIDS-related kidney problem? |
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| *focal segmental golmerulonephritis* seen in heroin using/HIV pts |
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| what are some cardiac manifestations of HIV? |
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| myocarditis, infectious endocarditis, pleural effusions from tumors/lymphomas, premature atherosclerosis, action of rx protease inhibitors, pulm HTN |
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| how is the biliary system affected by HIV? |
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| CMV/cryptosporidium can cause acalculous cholecystitis, duct problems, pancreatitis, NHL |
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| what is commonly seen with HIV pts' skin? what does it form? what can it resemble? |
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| kaposi's sarcoma, very aggressive, involves blood vessels and can form plaques/patches, poorly formed vascular channels. bacillary angiomatosis can look like kaposi's, but is caused by baronella henslae |
