- RNA virus with 3 groups 1) group specific Ag 2) reverse transcriptase and integrase 3) envelope codes to envelope proteins

- any age group - less common in kids than ALL - Auer rods seen

- middle aged pts - Ph + - 70% change to ALL/AML (when this happens they are dead within a year)

final Flashcards by JOSH WOHL

B lymphocytes are derived from

BM stem cells

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B cells mature into

plasma cells that secrete IGs

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MC IG?

IgG

IgA is in the gut

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these IGs are seen in hypersensitivity rxns

IgD/IgE

two heavy and light chains

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what is complement

-Lysis of bacteria or blood cells
-opsonize (coat) bacteria/blood cells for phagocytosis
-Immunoglobulins presenting to T-cells
Develops in the spleen, fully developed by 5-6 years of age (we don’t want to remove spleen before this)

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AIDS

RNA virus with 3 groups
1) group specific Ag
2) reverse transcriptase and integrase
3) envelope codes to envelope proteins

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when an infected HIV cell goes into replicative phase what is happening?

the provirus will produce mRNA and RNA to create new HIV virions

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normal CD4+ count vs AIDS count

normal-800-1000

AIDS-<400

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which cells does HIV infect?

CD4 (helper T cells)

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how to dx AIDS?

ELISA
Western Blot
may nto be positive for 3 months after exposure

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how to treat AIDS?

HAART (higly active anti-retro viral therapy)

type reverse transcriptase inhibitors and a protease inhibitor

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Diploid
Haploid
Aneuploid
Hyperdiploid
Hypodiploid
Psuedodiploid

Diploid = 46 chromosomes
Haploid = 23 chromosomes
Aneuploid = more or less than 46 chromos.
Hyperdiploid = more than 46 chromosomes
Hyplodiploid = less than 46 chromosomes
Pseudodiploid = 46 with chr rearrangement

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tumor suppressor genes inhibit cell division. Loss of one allele may predispose to certain tumors suh as

retinoblastoma

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Philadelphia Chromosome + in ALL indicates

hyperdiploidy in ALL indicates

poor prognosis

favorable prognosis

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Blast cells fail to differentiate but divide - result is bone marrow failure

acute leukemia

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MC form of leukemia in children (3-5)

acute lymphoblastic leukemia
-CD 10+ precursor B type is a marker on the cell that shows equal sex distribution
-CD 10- T type is MC in males
If kid keeps get sick every few weeks, then after a while they have swollen lymph nodes/spleen/liver
Blood count smear will be full of blasts, then do a bone marrow (normal person would have 5% blast cells,25-40%)
Liver/spleen can start to make red cells which causes them to get bigger

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AML is seen in

any age group
less common in kids than ALL
Auer rods seen

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M0-M7 classification is used for

AML

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FAB classification is used for

ALL

mediastinal lymph nodes are common with ALL

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Breaking tumor cells down releasing all intracellular contents into blood

tumor lysis syndrome, give allopurinol

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when to perform BMT on ALL vs AML

ALL- second remission

AML-first remission

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CML is seen in

middle aged pts
Ph +
70% change to ALL/AML (when this happens they are dead within a year)

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when do CML pts need a transplant by?

age 55

CLL is mainly seen in

adults
Mikulicz’s Syndrome = salivary & lacrimal inability to produce these fluids
doesn’t transform into acute

Reed Sternberg cells are seen in

Hodkins disease

how does Hodkin's present?

Present with painless, non-tender, asymmetrical enlarged superficial nodes, fever, weight loss, night sweats

this histological finding shows the best prognosis for Hodgkin's

lymphocyte predominance

stages of Hodkins

1-one set of lymph nodes 2-2 sets of lymph nodes on same side of body 3-lymph nodes above and below diaphragm 4-outside involvement B indicates fever, night sweats, weight loss (10%) - over 6 mos S indicates splenic involvment

hwo to dx hodgkins

- CXR - Bone Marrow - CT

hodgkin's treatment?

stage I and IIa get radiation | stage IIb, III, IV get radiation and chemo

NHL is a disease of which cells?

B lymphocytes

presentation of NDL

Anemia, neutropenia (infections), thrombocytopenia (purpura) Hepatosplenomegaly (organ involvement) Enlarged mesenteric/retroperitoneal nodes

NHL prognosis is based on

histology

HDL tx?

autologous marrow transplant to cure patient if radiation or chemo doesn't work

Burkitt's

B-lymphoblastic lymphoma Massive jaw lesions, extranodal abdominal & ovarian involvement in African children “Starry Sky”

Multiple Myeloma

-Proliferation of BM plasma cells -Lytic bone lesions (holes in the bone) -Bence Jones protein/paraprotein ex-person walking and falls, has a fracture

clinical features of MM

- bone pain - anemia - repeated infections

how to dx MM?

- alk phos - High BUN (higher the BUN, less life expectancy) - renal failure

how to tx MM?

- chemo - allopurinol - BMT for younger

polycthemia vera

- increased RBCs | - Becomes sludgy/sticky and plugs up vessels in brain causing HAs, blurry vision, dyspnea

secondary polycythemia

-compensatory increase in erythropoieten from -higher altitudes -cardiac disease pulmonary disease

Kid w/rash on butt down to feet Vessels break leading to bruises The kid is fine, make sure to test urine and guaiac for bleeding Treat with steroids, usually self limiting

Henoch-Schoenlein Syndrome Immune complex hypersensitivity reaction Usually children following an acute infection

hemolytic uremic syndrome is caused by

- E. Coli - pt presents with bloody diarrhea - treat with plasmapharesis and plasma transfusion

ITP

Idk why but you have no platelets Typically follows infection, abs are continued to be made and they attack platelets Occurs in the spleen, can remove the spleen and this will cure, increases platelet count a SHIT ton Rash doesn’t blanch No treatment necessary just follow the platelets, can give steroids and taper, above 30/40k then leave it alone IV IG in the hospital will cure Rh+ give rhogam

intrinsic pathway activates factor

XII--->XI--->IX---->vWF + VIII----->X

extrinsic pathway activates factor

VII----->X | crush injury will activate this

factor X becomes....

prothrombin which turns into thrombin | fibrinogen which turns into fibrin

fibrin degradation product is called

d-dimer

hemophilia a

missing factor VIII

how to treat hemophilia A

Give the recombinant medication every day via IV for a normal life

hemophilia b -christmas disease

missing factor IX

how to treat hemophilia b?

This is blood bank stuff, no manmade med | Given every second or third day

VWD

- autosomal dominant - MC general hemophilia - helps protect factor XIII - Platelets don’t function properly, don’t close up the hole

From sepsis, meningitis, etc | Clotting everywhere! Put person on heparin

DIC

DIC triad

- thrombocytopenia, decreased fibrinogen, increased split products (FDP)