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Heme II > Hematopoiesis and benign conditions > Flashcards

Hematopoiesis and benign conditions Flashcards

1
Q

HSC

A

during 3rd month migrate to liver
also take up residence in fetal placenta (can be harvested)
by 4th month reside in marrow
after puberty hematopoiesis restricted to axial skeleton

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2
Q

GFs of very early committed progenitors

A

Stem cell factor (KitL)

FLT3-L

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3
Q

GFs of committed progenitors

A

erythropoietin
GM-CSF
G-CSF
Thrombopoietin

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4
Q

Bone Marrow

A

thin walled sinusoids
lined by single layer of endothelium
discontinuous BM and adventitial cells
hematopoietic cells and fat cells 1:1

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5
Q

megakaryocytes

A

lie next to sinusoids and extend cytoplasmic processes that bud off into blood stream

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6
Q

nurse cells

A

surround RBC precursors

are specialized macrophages

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7
Q

leukoerythroblastosis

A

process which disrupts architecture of marrow causing abnormal release of immature precursors into periphery

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8
Q

sequence of RBC production

A

proerythroblasts -> basophilic erythroblast -> polychromatophilic erythroblast -> nucleated red cells -> reticulocyte -> mature erythrocytes

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9
Q

proerythroblast

A

large round cell
mild basophilia
only in marrow

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10
Q

basophilic erythroblast

A

smaller
deeply basophilic
only in marrow

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11
Q

polychromatophilic erythroblast

A

basophilic ribosomes
eosinophilic cyto
only in marrow

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12
Q

nucleated red cells

A

should only in marrow

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13
Q

normal MCV

A

80-100

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14
Q

RBC normal

A
  1. 1-5 men

3. 5-5 women

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15
Q

normal platelets

A

150-450

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16
Q

normal WBC

A

4.8-10.8

granulocytes 40-70%

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17
Q

disease states associated w/ineffective hematopoiesis

A

megaloblastic anemia

myeloid dysplastic syndrome

18
Q

immunologically mediated injury to neutrophils

A

idiopathic
SLE or other autoimmune conditions
drugs

19
Q

most common cause of agranulocytosis

A

drug toxicity

alkylating agents and antimetabolites used in chemo

20
Q

infections due to agranulocytosis

A

ulcerating necrotizing lesions of oral cavity characteristic
can progress to death in hours to days
high risk for candida and aspergillus
most serious when neutrophils <500

21
Q

leukocytosis

A

increase in WBCs

22
Q

acute infection leukocytosis

A

may be due to TNF and IL1

23
Q

prolonged infection leukocytosis

A

TNF and IL1 stimulate macros, bone marrow stromal cells, T cells -> produce hematopoietic GFs `

24
Q

IL5

A

eos

25
Q

G-CSF

A

neutrophils

26
Q

leukocytosis neutrophil changes

A

toxic granulations
Dohle bodies
cytoplasmic vaculoles

27
Q

Toxic granulations

A

coarser and darker then normal granules

abnormal azurophilic granules

28
Q

Dohle bodies

A

patches of blue dilated ER that appear as sky-blue cytoplasmic puddles

29
Q

neutrophilic leukocytosis

A

actue bacterial infections

30
Q

esosinophilic leukocytosis

A 
allergic disorders
parasitic infections
drug rxns
malignaces (NHLs and HLs)
autoimmune disorders
vasculitides
31
Q

basophilic leukocytosis

A

rare

MPD

32
Q

Monocytosis

A 
chronic infections (TB)
bacterial endocarditis
ricketsial and malaria
autoimmune
33
Q

lymphocytosis

A

chronic infections

viral infections

34
Q

follicular hyperplasia

A

due to activation of humoral response
RA
Toxoplasmosis
early HIV

35
Q

follicular hyperplasia morphology

A

dark zone
light zones
DCs
tangible-body macrophages

36
Q

reactive hyperplasia

A

preservation of lymph node architecture
frequent mitotic figures
phagocytic macros
light and dark zones

37
Q

paracortical hyperplasia

A

due to activation of T-cell mediated immune response

38
Q

sinus histiocytosis

A

aka reticular hyperplasia

increase in number and size of cells that line lymphatic sinusoids

39
Q

tertiary lymph organs

A

chronic immune rxns promote appearance of organized collections of immune cells in non-lymphoidal tissue
H.pylori at peyers patches
RA in inflamed synovium
due to lymphotoxin

40
Q

HLH

A

hemophagocytic lymphohistoiocytosis
aka macrophage activation syndrome
can be familial appearing early in like triggered by infection (EBV)
marked cytopenia and systemic inflammation

41
Q

HLH pathogenesis

A

activation of macros and CD8 T cells -> release mediators -> suppress hematopoiesis and produce systemic inflammation -> cytokine storm -> shock like syndrome

42
Q

HLH presentation

A

acute febrile illness
splenomegaly and hepatomegaly
hemophagocytosis in bone marrow
rapidly progress to shock and death

Heme II (7 decks)

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