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79 Cards in this Set

  • Front
  • Back
Neutrophil
The Phagocyte (has anti-microbials, most--abundant)
Eosinophil
The Parasite Destroyer, Allergy Inducer
Basophil
The Allergy Helper (IgE receptor=> histamine release)
Monocyte
The Destroyer=> MP (hydrolytic enzymes, coffee-bean nucleus)
Lymphocyte
The Warrior => T, B, NK cells
Platelets
The Clotter (no nuclei, smallest cells)
Naming Pattern
--------blast
Pro-----cyte
--------cyte
Meta---cyte
Blast:
baby hematopoietic cell "Blast them all"
Band
baby neutrophil (has maximal killing power)
Embryology of Hematopoietic Cells: how do RBC grow?
>>Blood Dwellers:
>>Normoblast ⇨ Reticulocyte ⇨ RBC
Embryology of Hematopoietic Cells: how do platelets grow?
Blood Dwellers
Megakaryoblast ⇨ Platelet "big to little"
Embryology of Hematopoietic Cells: how do macrophages grow?
Blood Dwellers:
Monoblast ⇨ Monocyte ⇨ MP
Embryology of Hematopoietic Cells: how are Tcells, B cells made
Tissue Dwellers:
Lymphoblast ⇨ Lymphocytes ⇨
• NK cells
• T cells (T H=CD4, T K=CD8)
• B cells=> plasma cells
Embryology of Hematopoietic Cells: how do PMN's, Eosinophils and basophils grow?
Myeloblast ⇨ Band "stab" cell ⇨ WBC "leukocyte" ⇨ Granulocytes:
• PMNs = "neutrophils"
• Eosinophils
• Basophils =>mast cells
what is demargination?
90% of WBC are marginated along blood vessels (most are mature), 10% are in circulation
Under extreme stress the body will demarginate even immature WBC
what compounds can cause demargination?
what happens to the levels of eosinophils, t cells and PMNs?
Steroids/Cortisol/Epi => demargination (w/ low eosinophils, low T cells, high PMNs)
describe the steps of demargination?
what is involved in step 1
what causes step 2
1) Pavementing:
Selectins: select mature WBC out of circulation
Integrins: (via ICAM-1) integrate WBC into endothelium
2) Margination= flatten (Epi and cortisol cause this)
3) Diapedesis = moves like a slinky looking for a break in endothelium
4) Migration = slide into the tissue
what Viruses can cause decreased WBCs "Leukopenia"?
Parvo B-19, Hep E, Hep C
Decreased WBCs "Leukopenia" Drugs?
AZT, Benzene, Chloramphenicol, Vinblastine
+High PMNs: Dx
"Stress demargination"
+Blasts (<5%): Dx
"Leukemoid Rxn =extreme demargination, looks like leukemia" (Ex: burn pt)
+Blasts (>5%): Dx
Ieukemia
+ Bands (immature neutrophils, max germ-killing ability): Dx
"left shift" = > have Infection
what is Agranulocytosis? and what drug causes them?
( ⇩WBC):
• Carbamazepine
• Ticlopidine
• Clozapine
• PTU
what is the earliest sign of agranulocytosis?
stomatitis is earliest sign
what would the levels of RBC, WBC
and platelets of Myelodysplastic
Syndromes be like
⇧stem cells => ⇧ RBC, WBC, platelets
what are the Myelodysplastic Syndromes
Polycythemia Rubra Vera
Essential Thrombocythemia
Myelofibrosis
Aplastic anemia
Polycythemia Rubra Vera:
pathogenesis
associated syndromes (4)
Tx
>>Hct >60%, ⇩Epo, ''puritis after bathing"
>>Gout, splenomegaly, ruddy appearance/cyanosis
>>Tx: Phlebotomy
Essential Thrombocythemia
describe and what does it lead to?
stain and what does it lead to?
Plt > 600k ⇨ stroke/DVT / PE/MI
stainable Fe, ⇨decreased c-mpl (TPOr)
Myelofibrosis:
pathogenesis
cells
prognosis
fibrotic marrow => teardrop cells, extramedullary hematopoiesis, poor prognosis
Aplastic anemia:
pathogenesis
lab
bone marrow replaced with fat, low retics
drugs that can cause Aplastic anemia:
AZT, Benzene , Chloramphenicol, Vinblastine
Viruses that can cause aplastic anemia:
Parvo-B-l9, Hep E, Hep C
Plasma Neoplasms:
pathogenesis
name all 3 diseases
>>produce lots of Ab
>>ie.Waldenstrom
Macroglobulinemia
Monoclonal Gammopathy of Undetermined Significance
Multiple Myeloma
Waldenstrom Macroglobulinemia:
Ig
spike
IgM, hyperviscous, M spike
Monoclonal Gammopathy of Undetermined Significance:
define
presentation
old people w / gamma spike
• peripheral neuropathy
Multiple Myeloma:
presentation, Ig, urine, RBC, prognosis, xray
>>old people with back pain
• Multiple "punched out" osteolytic lesions
• IgG--(M-spike)
• mu light chain (Bence-Jones proteinuria)
• Rouleaux
Multiple myeloma prognosis
albumin, vascularity, Ca, LDH, IL-6, Creatinine
has poor prognosis:
⇩albumin, ⇧vascularity, ⇧Ca, ⇧LDH, ⇧IL-6, ⇧Creatinine
MM 3 Dx test:
Serum protein electrophoresis, bone marrow biopsy,
skeletal survey
MM Tx:
Melphalan + Prednisone
Histiocyte (MP) Neoplasms:
Langerhans Cell Histocytosis "Histocytosis X": 4 clues
• Kids w / eczema, "punched out" skull lesions
diabetes insipidus
exophthalmos
what compound is toxic to leukemia cells
Arsenic is toxic to leukemia cells
what are the Leukemias?
Acute
Chronic
Myeloid
Lymphoid
Acute
started in bone marrow, squeezes RBC out of marrow
Chronic
started in periphery, not constrained => will expand
Myeloid leukemia
what cells are involved
test
⇧RBC, WBC, platelets (⇩lymphoid cells) =>do bone marrow biopsy
Lymphoid leukemia
what cells are involved
test
⇧NK, T, B cells: (⇩myeloid cells) => do lymph node biopsy
what is the most common leukemia?
ALL
which leukemia has the worst prognosis?
AML
which of the leukemias has the best prognosis
CLL
ALL/AML/CML/CLL
Age
Gender
ALL/AML/CML/CLL
age: 0-15/ 15-30/ 30-50/>50
gender: Male/ Male/ Female/Male
2 subtypes of ALL
which one has a bad prognosis?
Morphologic:
Ll: scant cytoplasm
L2: irregular nuclei
L3 = B-ALL
Phenotypic:
B-ALL: TdT(-)
T-ALL: mediastinal mass (bad)
3 subtypes of AML
M3 "Promyelocytic Leukemia" t(15;17)
M5: bleeding gums
M7: Down's, anti-platelet ab
3 subtypes of CML
a) Chronic: ⇧WBC
b) Accelerated: ⇩RBC,⇩platelets
c) Blastic:⇧blast cells, Red plaques
tx for AML M3
Tx: Retinoic Acid
subtype of CLL and average survival.
Diffuse lymphadenopathy
Average survival: 3 yrs
DX: Infxn: Bacterial
Bleeding/ petechiae
Teardrop cells
Low energy state
Bone pain
Thrombocytopenia
AML and ALL
presentation of CML
Go everywhere macrophages go
presentation of cells in CLL
Small mature
lymphocytes,
"soccer ball"
nuclei
5 markers : AML
which one indicates good chemo response?
which one indicates bad prognosis?
which one indicates good prognosis?
PAS stain ( + )
TdT ( + )
Calla ( + ) = > good chemo response
t(4,11): bad prog
t(12,21): good prog
markers: ALL
Sudan Stain
Auer rods (M3)
MPO
3 markers: CML
t(9 ,22) ·"Philadelphia chromosome"
bcr-abl
⇩LAP
3 markers: CLL
which one has good prognosis
CD 19,20
Smudge cells = fragile WBCs.
Mutated Vh genes: good prog
AML and ALLTx:
daunorubicin
CML tx:
Imatinib "Gleevac"
CLL tx:
Chlorambucil
Lymphomas: presentation
recurrent uticaria and eosinophilia
Hodgkin's: age range
20-40 y/o
Non-Hodgkin's:
who is at risk
location
what is increased?
ileum (⇧lymphoid tissue), affects
immunocompromised
Pathology Staging: hodgkins
what stage has a 90% cure
what is A
what is B
I: 1 group of lymph nodes
II: 2 groups (same side of diaphragm, 90% cure)
III: 2 groups across diaphragm
IV: metastasis (lymph node => organ)

A = without symptoms
B = sx: weight loss, fever, night sweats
Pathology Staging: non- hodgkins
Histology Staging:
I: limited to first layer
II: second layer
III: local invasion
IV: metastases
what should you check for for non-hodgkins lymphoma
Colon Cancer => do colonoscopy
HIV => ELIZA
4 common types of hodgkin's lymphoma
which one has the best prognosis?
which one has the worst prognosis?
which one has the low Reed strenburg cell?
EBV
a) Lympho Predom: best prognosis
b) Lymphocyte Depleted: worst prog
c) Mixed lymphocyte/ histiocyte
d) Nodular Sclerosis: low RS
2 B-cell: most common Types of non-hodgkins lymphomas
tranlocation
markers
biopsy
virus
Follicular: t(14,18), bcl2
Burkitt: t(8, 14), c-myc, starry MP, EBV
what indicates a poor prognosis in hodgkins lymphoma? and tx
Albumin <4: poor prognosis
tx; MOPP or ABVD
Reed-Sternberg
describe
CD
type of cells
B cells with bad Ig,owl's eyes, CD30, lacunar cells
Tcell non hodgkins lymphoma: 2 types and describe
describe each
T -cell: rare
Mycosis Fungoides: "bathing suit" rash
Sezary syndrome: cerebriform cells = MF
mets to blood
two types of burkitts lymphoma and which one has a poor prognosis?
• American kids: abdominal mass
• Poor: jaw mass
ChemoTx: hodgekins and non-hodgekins
Hodgekins: MOPP or ABVD
NH: CHOP