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Neoplasia Block > MOD 2 more lectures (Pathology of AIDS/HIV, and Intro to Hematolymphoid neoplasia) > Flashcards

MOD 2 more lectures (Pathology of AIDS/HIV, and Intro to Hematolymphoid neoplasia) Flashcards

1
Q

AIDS facts

A

mostly africa, then asia
top three cities for AIDS are Miami, NOLA, baton rouge
risk groups are homo/bi men, IV drugs (sometimes transfusion or newborns with HIV mothers)

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2
Q

AIDS routes of transmission

A

Sexual (75%)
perenteral (IV drug)
mother to infant

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3
Q

which route of transmission has highest rate of transmission of HIV (highest infectivity rate)?

A

transfusion of blood products bc highest viral load/conc

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4
Q

Key target of HIV virus?

A

CD4+

also types of macros bc cells with CD4 receptors

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5
Q

What type of viruses are HIV1/2?

A

nontransforming human retrovirus of LENTIVIRUS family

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6
Q

HIV-1 virion

A

2 single stranded copies of RNA
uses RT
has p24 capsid, use to ID (also ab’s to surface glycoprots)

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7
Q

HIV viral attachment and entry?

A

viral glycoprot gp120 binds CD4+ receptor
-interaction with chemokine receptor (co-receptor, eitehr CCR-5 of CXCR-4) exposes viral gp41(which can penetrate host memb bc lipophilic), membranes fuse and release viral contents into cyto

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8
Q

HIV viral replication

A 
HIV can either remain dormant in host cell (hard to target virus infected cells)
or cDNA (DNA synth from viral RNA using RT) can inc into host DNA (progressive infection)
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9
Q

What two things are needed for progressive infection?

A

actively dividing host cell

integrase (enz encoded by virus to integrate cDNA into host DNA)

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10
Q

What are the 3 stages of the HIV virus

A

Acute prodromal phase
Chronic stage
Crisis

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11
Q

Acute prodromal phase

A

nonsepc sx, drop in CD4 cells (T cells destroyed by many diff methods), viremia (widespread dissem of virus)

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12
Q

Chronic stage

A

clinical latency, no sx, immune cells being repl at same rate, enlarged lymph nodes due to lots of cytokine release

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13
Q

Crisis sx

A

constitutional sx (fever/chills/night sweats/ wasting) neoplasm, neuro disease, atrophic lymph nodes, opportunistic diseases

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14
Q

What happens to immune cells in HIV infection? Lymphoma?

A

decr T cell immune surveillance, decr B cell stim, abnormal lymphoid prolif due to cytokine stim (can progress into lymphoma which prod abnormal prots)

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15
Q

What is PGL (persistent generalized lymphadenopathy?)

A

nodal enlargement in extra-inguinal sites that lasts more than 3 months w/ constitutional sx (eg hepatosplenomeg, anema, hyper Igs)

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16
Q

Histo findings of PGL

A
  • follic hyperplasia (expanded irreg germinal ctr, T cell zone compressed, look like “naked follicles”)
  • dissolution of cortical germinal centers: follic DCs are infected, and their lysis causes germ ctr to fall apart (specific to HIV)
  • Lymphoid depletion: atrophic, w hyalinized germinal ctr
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17
Q

How can HIV cause cancer?

A

polyclonal to oligoclonal (few cell lines) to MONOCLONAL (one cell line) prolif

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18
Q

What is HIV assoc NHL (non-hodkins lymphoma?)

A

30% of aids pts get it, less prevalent w HAART use (highly active antiretroviral tx), B cell phenotype
-path: infxn with HIV causes immunosuppr, promotes infxn of EBV virus, potent mitogen causes prolif o fhost cells, mutations (e.g.. dereg of c-myc protooncogene in EBV, 8:__ transloc)

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19
Q

Subtypes of NHL lymphoma?

A

Diffuse large B cell lymphoma
Burkitt lymphoma
(both aggro)
Cavity based primary effusion lyphoma

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20
Q

What is cavity based lymphoma related to?

Sx?

A

EBV and HSV-8

early involvement of pleural spaces

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21
Q

Burkitt lymphoma histo?

Dx?

A

Lymphoid like cells larger than RBC and have cytoplasm vacuoles
Dx: IHC to confirm lymphoid origin

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22
Q

Kaposi sarcoma classic pres

A

indolent (slow onset, few sx), skin lesions

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23
Q

AIDS assoc kaposi sarcoma

A

STI indep of HIV, men
more aggro
HHV-8 and HIV synergise to affect cells of endoth origin, not just skin can inv any organ (lesions are epidermal mucocutaneous, and visceral)

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24
Q

What disease is kaposi sarcoma often associated with?

A

AIDS

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25
Q

Kaposi sarcoma pathology

A

rel of cytokines and GFs from infected cells, prolif of endoth cells and angiogen, vascualrize KS lesions

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26
Q

Kaposi sarcoma pathway

A

PATCH (flat red/purp macula) –> PLAQUE (thickning of patch) –> TUMOR (nodule)

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27
Q

What will biopsy of kaposi sarcoma lesion show>

A

spindle to epith atypical endoth cells, dilated vasc spaces, leaked or degraded RBCs which can lead to hemosiderin (brown) granules and hyaline bodies, inflam infiltrate

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28
Q

How can HIV promote squamous cell carcinoma of uterine cervix and anal canal?

A

synergy between HIV and HPV promotes neoplastic changes

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29
Q

HIV squamous cell carcinoma histo?

A

characterized by KOLIOCYTES (binucleated raisin nuclei with halo)

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30
Q

What do koliocytes on slides mean?

A

HPV infection

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31
Q

Viral infections common in AIDS patients (list)

A 
CMV (wtih low CD4 count, owl's eye inclusions)
HSV
varicela 
EBV
KSHV (HHV-8)
etc
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32
Q

Protozoal infections common in AIDS

A

Toxoplasma gondii (brain)
crytospor
microspor
isospor (latter 3 GI)

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33
Q

bacterial infections common in AIDS

A

mycobacterium TB and avium

bartonella

34
Q

fungal infections common in AIDS

A

PCP (lung eosin material, pneumonia sx)
candida (dissem inv solid organ abcesses)
histoplasma capsulatum (in macros)
coccidiodes (large cyst)
cryptococcus neoformans: asymp infects resp, spreads to CNS as meningitis (mucicarmien stain, india ink for capsule)

35
Q

HIV/AIDS and CNS infections

A
  • many CNS issues
  • pathogens include cryptococcus, CMV, toxoplasma
  • AIDS dementia complex
  • HIV encephalitis carried across BBB by infected monos/macros, infects a bunch of cells in brain, causes perivascular microglial nodules (aroudn bv’s)
  • Progressive Multifocal leukoencephalopathy: patchy areas of WM destruction, demylelination (on microscope: spaghetti and meatballs form of papovavirus/polyomavirus)
  • Toxoplasma encephalitis (protozoal infxn that resembles TB, lymphoma, intracranial mass with ring enhancement, non-spec; acute is necrotizing microabcesses in brain, chronic is microcysts)
36
Q

Diff between complete blood cell count (CBC) and differential blood count?

A

Differential gives percentages of WBCs, and CBC gives actual values of many diff blood cells.
“penia”= deficiency
“cytosis”= extra

37
Q

How do you measure “cellularity” of patient? (eg in bone marrow histology(?)

A

Normal cellularity is 100 minus age of patient
So 40 y.o. pt would have 100-40= 60% cellularity (40% fat)
So cellularity decreases, and fat increases, as u get older

38
Q

What progenitor cell gives rise to lymphocytes, and what gives rise to all other blood cells?

A

Myeloid stem cells give rise to myeloblasts (baso/eosin/neutro), monocytes, megakaryocytes, and pronormoblasts (RBCs)
Lymphoid stem cells give rise to lymphocytes (T, B, NK)

39
Q

What are 3 types of myeloid lineage diseases?

A
  1. Acute Myeloid Leukemia (AML)
  2. Myelodysplastic Syndrome (MDS)
  3. Myeloproliferative Neoplasms (MPN)
40
Q

AML (Acute myeloid leukemia)–which cells prolif?
Characteristics of these cells?
What main structural feature do only they have?

A

IMMATURE MYELOID BLAST CELLS in bone marrow:
int sized, round, blue cells, high N:C ratio, finely dispersed chromatin, nucleoli (white areas)
-Have AUER RODS: crystal aggregates of MPO (red lines) means abnormal mitosis

41
Q

AML
pop
dx
sx

A

slight male >65
DX BY MORE THAN 20% BLASTS IN PERIPH BLOOD OR MARROW
sx: anemia (fatigue, pallor), neutropenia, thrombocytopenia (bleeding)

42
Q

What’s an important type of AML?

Presentation? translocation?

A

ACUTE PROMYELOCYTIC LEUKEMIA (APL)
presents with dissem vascular coag (DIC, too much clotting, but can also bleed)
15;17 translocation

43
Q

MDS (myelodysplastic syndrome)
Cx
Risk of dev?
Diff w/ AML

A

CYTOPENIAS, dysplasia in myeloid line(s), ineffective hematopoeisis

  • incr risk of dev AML
  • must have LESS than 20% blasts (AML would be more than 20%)
44
Q

MDS
pop
sx

A
  • older ~male med age 70

- same 3 as AML

45
Q

MDS histology

A

high cellularity and incr megakaryocytes

  • left shift (incr monolobed neutros)
  • RING SIDEROBLASTS (iron Fe3+ stain allows us to see accum of stored iron, blue rings around pinkish cells)
46
Q

Cytopenia plus what genetic abnormalities may indicate MDS?

A

cytopenia + deletion of chrom 5q

47
Q

(MPN) Myeloproliferative Neoplasms
mutation
pop
marrow cells

A

Chronic prolif of MATURE cells (effective hematopoeisis–aka just too many)

  • Tyrosine kinase mutations can cause oncogenic growth
  • adults
  • hyper-cellular bone marrow with increased periph counts
48
Q

What can MPN develop into

A

Spent phase: hyper-prolif exhausts bone marrow, so dev cytopenia and marrow fibrosis
-can also transform into AML

49
Q

Which two myeloid diseases can become AML?

A

MDS and MPN

50
Q

What are 4 types of MPNs?

A 
Chronic myelogenous leukemia (CML)
Polycythemia Vera (PV)
Essential Thrombocytopenia (ET)
Primary Myelofibrosis (PMF)
51
Q

What mutation do the latter 3 (PV, ET, and PMF) all have?

A

JAK2 kinase mutation

52
Q 
CML
prolif
mut
tx
can become
A

GRANULOCYTE/BASO PROLIF, 9;22 bcr-abl fusion
Tx with imatinib
-can become AML or ALL

53
Q

PV
prolif
mut
sx

A 
RBC PROLIF (and granulo/platelets) (EPO dep erythrocytosis)
JAK2 kinase, hyperviscosity of blood, blurry vision, flushed face, itching, decr EPO, normal SaO2
54
Q

ET

prolif

A 
PLATELET PROLIF (also RBCs/gran)
jak2 kinase
55
Q

PMF
prolif
histo

A

MEGKARYOCYTE PROLIF
Jak2 kinase
PDGF leads to marrow fibrosis
TEAR DROP SHAPE OF RBCs on histo (darocyte) from distortion of memb from fibrosis

56
Q

other causes of neutrophilia (for differential dx)

A

bacteria, GF tx, stress

57
Q

other causes of thrombocytosis

A

iron def anemia, infxn, stress

58
Q

other causes of erythrocytosis

A

tumor (pheo, hepatic, ut leiomyo, cerebell hemangioblast, kidney), high alt, smoking, hypoxia, high O2 aff hb, blood doping or high T, INCR EPO LEVELS

59
Q

Diff between erythrocytosis due to PV vs other factors

A

PV shows DECREASED EPO, others show incr

60
Q

Which tumors causes erythrocytosis? (mnemonic)

A

PHUCK

61
Q

What can thymic mass indicate

A

T cell leukemia/lymphoma

62
Q

The two lymphoid neoplasia types are?

A

LEUKEMIAS and LYMPHOMAS

63
Q

Acute lymphoblastic leukemia (ALL)
pop
histo

A

Neoplasm of IMMATURE lymphoid precursors

  • often in kids
  • similar histo to AML but no Auer rods
64
Q

B-cell vs T-cell ALL?

A
  • B-cell ALL is more common (presents as acute leukemia inv marrow)
  • ALL presents as lymphoma inv anterior mediastinum
65
Q

Lymphomas in general

A

neoplasm of MATURE lymphoid cells

-most inv B cell

66
Q

Diff between leukemia and lymphoma

A

Leukemia is IMMATURE neoplasm, lymphoma is MATURE

67
Q

2 types of lymphomas?

A

Hodgkins and Non-Hodgkins

68
Q

Hodgkins lymphoma

  • cell dist feature
  • tx
A

presence of REED-STERNBERG CELLS (multinuclear giant cells), aggro

  • curable w/ combo tx
  • many types
69
Q

What are some classical types of hodgkins lymphoma

A

Nodular sclerosis
Mixed cellularity
Lymphocyte rich
Lymphocyte depleted

70
Q

Non-Hodgkin lymphoma B cell types

A

B cell types:

small: slow, noncurable;
large: aggro, curable, localized (TYPES include DIFFUSE LARGE B CELL AND BURKITT)

71
Q

Non-hodgkin lymphoma T cell and NK cell types

A

aggro, curable, localized,

-types incl periph T cell, anaplastic large cell, adult t, mycosis fungoides, large gran, extranodal

72
Q

What 2 types o fmarkers are used to distinguish cell types in immunophenotypic analysis in lymphoid neoplasias?

A

Pan markers and Maturity markers

73
Q

Pan marker examples>

A

for B cells: CD19, CD20 (obv)

For T and NK cells: CD3

74
Q

Maturity marker examples

A

immature blast: TdT

myeloblast specifically: CD34

75
Q

What does lots of CD19 and CD20 indicate

A

B cells

76
Q

What does lots of CD34 indiccate

A

myeloblasts

77
Q

Genetic analysis methods in lymphoid issues?

A

Karyotyping, FISH, PCR

78
Q

Which lymphoid issue has greater than 20% blasts

A

AML!

79
Q

Which lymphoid issue has auer rods?

A

AML!

80
Q

Which lymphoid issue has ring sideroblasts w/ iron stain?

A

MDS (meylodysplastic syndrome, a myeloid neoplasia)

81
Q

Which lymphoid issue has reed-sternberg cells (multinuclear giant cells)

A

HODGKINS LYMPHOMA!

Neoplasia Block (16 decks)

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