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HEME/LYMPH Exam 1 > Chapter 13 Robbins > Flashcards

Chapter 13 Robbins Flashcards

1
Q

What can stimulate HSCs in marrow to move from stem cell niches?

A

G-CSF

Response to stress

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2
Q

Marrow response to short term needs

A

Controlled by growth factors that act on committed progenitors

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3
Q

Growth factors acting on EARLY committed progenitors

A

KIT ligand and FLT3-ligand

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4
Q

Growth factors acting on restricted progenitors

A

Erythropoietin, GM-CSF, G-CSF, and thrombopoietin

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5
Q

Distortion of marrow architecture can lead to

A

Abnormal release of immature precursors (leukoerythroblastosis)

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6
Q

Fat cells increase in bone marrow in

A

Hypoplastic states

And decrease in neoplastic or hyperplastic states

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7
Q

Leukopenia usually results from

A

Decreased number of neutrophils

Usually associated with decreased function of granulocytes

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8
Q

Lymphopenia most commonly from

A

HIV, glucocorticoid therapy, autoimmune disorders, malnutrition and viral infections

Usually a redistribution (to LN and tissue) rather than a decrease in number

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9
Q

Cause of neutropenia

A

Inadequate/ineffective granulopoiesis

Increased destruction/sequestions

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10
Q

Suppression of HSCs causing neutropenia

A

Aplastic anemia, tumors, granulomatous disease

Accompanied by anemia and thrombocytopenia

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11
Q

Suppression of granulocyte committed precursors causing neutropenia

A

Drug toxicity

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12
Q

Ineffective hematopoiesis causing neutropenia

A

Megaloblastic anemias, myelodysplastic syndromes (precursors die in the marrow)

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13
Q

Congenital syndromes causing neutropenia

A

Kostmann syndrome

Impairs differentiation of granulocytes

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14
Q

Immune mediated destruction of neutrophils

A

Can be idiopathic, associated with a disease like SLE, or drug toxicity related

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15
Q

Effect of splenomegaly on neutrophils

A

Increased sequestration

Sometimes associated with anemia and thrombocytopenia

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16
Q

Increased peripheral utilization of neutrophils occurs with

A

Bacterial, fungal and rickettsial infections

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17
Q

Most common cause of agranulocytosis

A

Drug toxicity
Red cells and platelets also effected

Aminopyrine, chloramphenicol, sulfonamides, chlorpromazine, thiouracil, and phenylbutazone

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18
Q

Chlorpromazine effect on neutrophils

A

Direct toxicity

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19
Q

Sulfonamide effect on neutrophils

A

Antibody mediated destruction

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20
Q

LGL leukemia effect on neutrophils

A

Monoclonal proliferation of lymphocytes suppresses production of neutrophils

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21
Q

Morphological consequences of neutropenia

A 
Compensatory marrow hyperplasia
Increased infections (candida and aspergillus)
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22
Q

Clinical features of neutropenia

A

Related to infection - serious infections when under count of 500
Fever, malaise, and chills

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23
Q

Peripheral leukocyte count

A

Size of precursor and storage pools
Rate of release into circulation
Size of marginal pool (adhering to BV)
Rate moving into tissues

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24
Q

Most important cause of neutrophilic leukocytosis

A

Infection

Mediated by IL-1 and TNF

25
Q

Increased production of neutrophils in marrow

A

Chronic infection or inflammation
Paraneoplastic
Myeloproliferative

26
Q

Increased release of neutrophils

A

Infection
Endotoxemia
Hypoxia

27
Q

Decreased margination of neutrophils

A

Exercise

Catecholamines

28
Q

Decreased extravasation

A

Glucocorticoids

29
Q

IL-5 specifically stimulates

A

Eosinophils

30
Q

G-CSF specifically stimulates

A

Neutrophils

31
Q

In sepsis or severe inflammation leukocytosis in accompanied by

A

Morphological changes in neutrophils
Toxic granulations
Dohle bodies
Cytoplasmic vacuoles

32
Q

Toxic granules

A

Appear coarser and darker

Abnormal primary granules

33
Q

Dohle bodies

A

Patches of dilated endoplasmic reticulum that appear as sky-blue cytoplas- mic “puddles”

34
Q

Reactive vs Neoplastic leukocytosis

A

Usually able to distinguish except in cases of acute viral infection in kids or severe infections leading to immature cells in the blood like in a myeloid leukemia (leukemoid reaction)

35
Q

Neutrophilic leukocytosis caused by

A

Acute bacterial

Sterile inflammation

36
Q

Eosinophilic leukocytosis caused by

A

Allergic disorders
Malignancy
AI disorders

37
Q

Basophilic leukocytosis is

A

Very RARE

Myeloproliferative disease

38
Q

Monocytosis caused by

A

Chronic infections
AI disorders
Inflammatory bowel disease

39
Q

Lymphocytosis associated with

A

Monocytosis

Viral infections

40
Q

Germinal centers

A

Pale staining, seen when primary follicles enlarge

B cells acquire capacity to make high affinity antibodies

41
Q

T cells in LN

A

Reside in paracortical zones

Undergo hyperplasia during immune response

42
Q

Acute nonspecific lymphadenitis

A

LN are swollen with large, reactive germinal centers
Pyogenic organisms -> neutrophils -> necrosis/pus

Seen more in cervical and mesentary

43
Q

Follicular hyperplasia

A

Chronic nonspecific lymphadenitis - Result of humoral response
**Tingible body macrophages
RA, toxo, HIV

(looks similar to follicular lymphoma but architecture is intact and everything more organized)

44
Q

Paracortical hyperplasia

A

Chronic - T cell response (viral infection)

T cell zones are bigger and contain immunoblasts (larger)

45
Q

Sinus histiocytosis

A

Seen in LN draining cancer (breast cancer)

46
Q

Chronic LN inflammation

A

Common in axillary and inguinal

LN are nontender and large/hard

47
Q

Tertiary lymphoid organs

A

Seen with chronic immune reactions
Immune cell collections in non-lymphoid tissue

Classic ex. include RA (B cells in joints) and chronic gastritis from helicobacter pylori

48
Q

Hemophagocytic lymphohistiocytosis (HLH)

A

Systemic activation of macrophages and CD8+ cytotoxic T cells -> cytopenia and shock (mediators initiate systemic inflammation)

Something to do with toxic granules of NK and cytotoxic T cells

49
Q

Most common trigger of HLH

A

EBV (infection)

50
Q

Clinical features of HLH

A

Acute febrile illness, hepatosplenomegaly
Anemia, thrombocytopenia, high levels of plasma ferritin and soluble IL-2 receptor
Treat with immunosuppressive therapy -> poor prognosis especially if not treated

51
Q

When are proto-oncogenes often activated in lymphoid cells?

A

Antigen receptor gene rearrangement and diversification

  • Increased AID expression -> induce MYC/Ig translocations
  • Increased expression of BCL6
  • Precursor B and T cells express VDJ recombinase -> cuts DNA
52
Q

Pro growth mutations

A

Tyrosine kinase

MYC

53
Q

Self renewal mutations

A

MLL translocation, PML-RARA fusion gene

54
Q

Pro survival mutations

A

BCL2 translocation

55
Q

Diseases that cause genetic instability

A

Bloom syndrome, Fanconi anemia, and ataxia telangiectasia (acute leukemia)

Downs and Type I NF (childhood leukemia)

56
Q

Lymphotrophic viruses

A

Human T-cell leukemia virus-1 (HTLV-1), EBV, and Kaposi sarcoma herpesvirus/human herpesvirus-8

57
Q

Chronic inflammation and lymphoid neoplasia

A

H. pylori -> gastic B cell lymphoma
Celiac and breast implants -> T cell lymphomas (local)
HIV -> germinal center B cell lymphomas (systemic)

58
Q

Radiation therapy and cancer

A

Increased risk of myeloid and lymphoid neoplasms

59
Q

Smoking and white cell cancer

A

Increased risk of acute myeloid leukemia

HEME/LYMPH Exam 1 (1 decks)

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